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Inflammation

Inflammation is a fundamental biological response of the immune system to harmful stimuli, including pathogens, damaged cells, irritants, or toxins, aimed at protecting the body by eliminating the cause of injury and initiating the healing process.^[1] This response involves localized changes such as vasodilation, increased vascular permeability, and recruitment of immune cells, leading to the classic cardinal signs of redness (rubor), heat (calor), swelling (tumor), pain (dolor), and sometimes loss of function.^[2] These signs arise from the release of mediators like histamine, cytokines, and reactive oxygen species, which coordinate the inflammatory cascade.^[1] Inflammation manifests in two primary forms: acute and chronic. Acute inflammation is a rapid, short-term reaction, typically lasting hours to days, dominated by neutrophils and aimed at quick resolution to restore tissue homeostasis.^[1] In contrast, chronic inflammation develops more slowly over weeks, months, or years, involving monocytes, macrophages, and lymphocytes, and often persists when the initial trigger is not fully eliminated or due to autoimmune dysregulation.^[3] While acute inflammation is generally beneficial for defense and repair, chronic inflammation can become detrimental, contributing to tissue damage and the pathogenesis of numerous diseases.^[4] The clinical significance of inflammation extends to its role in both health maintenance and disease progression, influencing conditions from infections to chronic disorders. For instance, unresolved inflammation is implicated in over 50% of global deaths, including cardiovascular diseases, diabetes, cancer, and neurodegenerative conditions like Alzheimer's.^[4] Environmental factors, such as air pollution and chemical exposures, can exacerbate inflammatory responses, heightening risks for asthma, heart disease, and even certain cancers.^[4] Elevated biomarkers like C-reactive protein (CRP) serve as indicators of systemic inflammation and predictors of adverse outcomes in these pathologies.^[1] Understanding inflammation's mechanisms has driven therapeutic advancements, including anti-inflammatory drugs like NSAIDs and biologics targeting specific cytokines.^[1]

Fundamentals

Definition

Inflammation is a fundamental protective response of the innate immune system designed to eliminate harmful stimuli, such as pathogens or damaged cells, and to initiate the healing process. This complex biological reaction coordinates the activation of immune cells, including neutrophils and macrophages, alongside changes in blood vessels and the release of molecular mediators like cytokines and chemokines to localize and resolve the threat.^[5] The hallmark clinical signs of inflammation, articulated by the ancient Roman encyclopedist Aulus Cornelius Celsus, encompass redness (rubor) due to vasodilation, heat (calor) from increased blood flow, swelling (tumor) caused by fluid accumulation, and pain (dolor) resulting from nerve irritation and pressure. A fifth sign, loss of function (functio laesa), was later incorporated by the physician Galen, reflecting impaired tissue utility during the response. These observable features underscore inflammation's role in alerting the body to injury while promoting repair.^[6] Inflammation manifests in two primary forms: local, which is restricted to the site of insult and typically resolves without broader impact, or systemic, which engages the entire organism through circulating mediators and can influence distant tissues.^[2] From an evolutionary perspective, inflammation emerged as an adaptive mechanism in multicellular organisms to defend against pathogens, physical injuries, and environmental toxins, thereby preserving tissue integrity and organismal survival across species.^[7]^[8]

Historical Context

The understanding of inflammation dates back to ancient civilizations, where early observers noted its observable signs without a mechanistic explanation. In the 5th century BC, Hippocrates, the Greek physician often regarded as the father of medicine, described inflammation in terms of tissue changes such as redness, swelling, heat, and pain, using terms like rubor (redness), tumor (swelling), calor (heat), and dolor (pain), which laid the groundwork for later classifications.^[9] These observations were empirical, derived from clinical experience, and emphasized inflammation as a response to injury or imbalance in bodily humors. By the 1st century AD, the Roman encyclopedist Aulus Cornelius Celsus formalized these into the four cardinal signs in his work De Medicina, providing a systematic description that influenced medical thought for centuries.^[10] The 19th century marked a shift toward microscopic and experimental investigations, revealing cellular processes underlying inflammation. In 1867, German pathologist Julius Cohnheim demonstrated leukocyte extravasation—the migration of white blood cells from blood vessels into tissues—through innovative intravital microscopy experiments on frog tongues and guinea pig mesentery, challenging earlier views of inflammation as merely a vascular event.^[11] Building on this, Ilya Metchnikoff advanced the cellular theory of immunity in the 1880s by discovering phagocytosis, the active engulfment of pathogens by leukocytes. Paul Ehrlich contributed through his novel staining techniques to visualize and classify leukocytes, supporting the understanding of their roles in immune defense.^[12]^[13] These contributions transitioned inflammation from a descriptive phenomenon to a process involving dynamic cellular movements. In the 20th century, biochemical discoveries illuminated the molecular mediators orchestrating inflammation. Prostaglandins, key lipid mediators, were first identified in the 1930s by Ulf von Euler from human seminal fluid and sheep prostate extracts, revealing their role in smooth muscle contraction and later in inflammatory responses.^[14] The 1970s and 1980s brought the isolation and characterization of interleukins and other cytokines, such as interleukin-1 (discovered as leukocytic pyrogen in the 1940s but molecularly defined in the 1980s) and interleukin-2 (identified in 1976 as a T-cell growth factor), which elucidated the signaling cascades amplifying inflammation.^[15] Cytokines, broadly recognized by the late 20th century, were shown to coordinate the inflammatory response through interconnected pathways.^[16] Mid-century research, particularly post-1950s advances in immunology, shifted emphasis from predominantly humoral theories—favoring soluble factors like antibodies—to cellular theories, integrating both but highlighting leukocytes and their mediators as central drivers.^[17]

Causes

Exogenous Causes

Exogenous causes of inflammation arise from external environmental factors that directly damage tissues or activate immune recognition, distinguishing them from internal physiological triggers. These factors encompass microbial invasions, physical injuries, and chemical exposures, each capable of initiating a protective inflammatory response to restore homeostasis.^[18] Microbial infections represent a leading exogenous inducer of inflammation, primarily through the recognition of pathogen-associated molecular patterns (PAMPs) on bacteria, viruses, fungi, and parasites by host pattern recognition receptors. Bacterial pathogens, such as Streptococcus pyogenes, provoke acute pharyngitis by adhering to throat mucosa and eliciting localized inflammation characterized by redness, swelling, and pain.^[19] Viral infections like influenza trigger robust respiratory inflammation via viral PAMPs, leading to symptoms including fever and airway hyperreactivity.^[20] Fungal agents, including Candida species, and parasitic organisms, such as helminths, similarly stimulate inflammatory cascades through their surface PAMPs, often resulting in tissue-specific responses like mucosal irritation or granuloma formation. For instance, bacterial obstruction of the appendix lumen, commonly by fecaliths harboring pathogens, causes acute appendicitis with intense localized inflammation.^[21] Physical agents induce inflammation via mechanical or thermal disruption of tissue barriers, prompting repair mechanisms. Trauma, such as cuts or blunt force, directly damages cells and vessels, initiating an inflammatory cascade to clear debris and promote healing. Burns from heat sources denature proteins and cause necrosis, leading to a graded inflammatory response proportional to tissue depth affected. Ionizing radiation generates free radicals that harm DNA and cellular structures, resulting in delayed or acute inflammation depending on exposure dose. Foreign bodies, exemplified by splinters or embedded debris, provoke persistent localized inflammation as immune cells encapsulate the intruder to prevent dissemination.^[18] Chemical irritants trigger inflammation through corrosive effects or hypersensitivity reactions, often affecting skin or mucosal surfaces. Strong acids and alkalis cause immediate tissue necrosis and secondary inflammation by disrupting cellular membranes and pH balance. Toxins from environmental sources, including heavy metals, induce oxidative stress and inflammatory mediator release. Allergens like urushiol, the oleoresin in poison ivy (Toxicodendron radicans), elicit type IV hypersensitivity, manifesting as allergic contact dermatitis with vesicular eruptions and intense pruritus.^[22] Similarly, nickel exposure in jewelry or tools commonly leads to chronic eczematous inflammation in sensitized individuals via hapten-mediated T-cell activation.^[23]

Endogenous Causes

Endogenous causes of inflammation arise from internal physiological disruptions or pathological processes within the body, distinct from external triggers, and often involve the release of endogenous molecules that alert the immune system to cellular damage or dysfunction. These factors initiate inflammatory responses through mechanisms such as the recognition of damage-associated molecular patterns (DAMPs), which are intracellular components released by stressed or dying cells and recognized by pattern recognition receptors on immune cells.^[24] Tissue necrosis represents a primary endogenous cause, where cell death due to ischemia or other internal insults leads to the liberation of DAMPs, thereby activating innate immune responses and promoting inflammation. For instance, in myocardial infarction, ischemic necrosis of cardiac tissue releases DAMPs such as high-mobility group box 1 (HMGB1) and mitochondrial DNA, which bind to receptors like Toll-like receptor 4 (TLR4) on macrophages and endothelial cells, initiating a cascade of cytokine production including interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α).^[25]^[26] This sterile inflammation can exacerbate tissue damage and contribute to complications like heart failure if unresolved. Autoimmune reactions constitute another key endogenous trigger, occurring when the immune system erroneously targets self-antigens, leading to persistent inflammation in affected tissues. In rheumatoid arthritis, for example, autoantibodies such as rheumatoid factor and anti-citrullinated protein antibodies (ACPAs) form immune complexes that deposit in the synovial joints, activating complement and recruiting neutrophils, which release pro-inflammatory mediators and perpetuate synovial inflammation. This dysregulated response involves T-cell activation and cytokine storms, particularly involving IL-6 and IL-17, driving joint destruction over time.^[27]^[28] Metabolic disturbances also provoke endogenous inflammation through the accumulation of aberrant metabolites that act as irritants to immune cells. Crystal-induced inflammation, as seen in gout, results from monosodium urate crystals formed due to hyperuricemia, which are phagocytosed by macrophages, activating the NLRP3 inflammasome and releasing IL-1β to cause acute joint inflammation. Similarly, in early atherosclerosis, oxidized low-density lipoprotein (oxLDL) accumulates in arterial walls, serving as a DAMP that stimulates endothelial cells and macrophages via scavenger receptors and TLRs, leading to foam cell formation and chronic vascular inflammation. These processes highlight how metabolic imbalances can initiate and sustain inflammatory states.^[29]^[30] Additional examples include pancreatitis, where premature activation of pancreatic digestive enzymes leads to autodigestion of acinar cells, releasing enzymes like trypsin that damage surrounding tissue and trigger local inflammation through protease-activated receptors and cytokine release. In inflammatory bowel disease, immune dysregulation in the gut mucosa results in aberrant responses to commensal antigens, involving overproduction of pro-inflammatory cytokines such as TNF-α and IL-23 by lamina propria T cells and innate lymphoid cells, causing chronic intestinal inflammation. Such endogenous mechanisms underscore the body's intricate balance in immune surveillance, where internal derangements can escalate into pathological inflammation.^[31]^[32]

Classification

Acute Inflammation

Acute inflammation represents a rapid, short-term defensive response of the innate immune system to harmful stimuli, such as pathogens or tissue injury, designed to eliminate the inciting agent and initiate repair processes. It typically onset within minutes to hours following the trigger and lasts for a few days, allowing for the containment and clearance of the threat while minimizing damage to surrounding tissues.^[18]^[1] The process begins with an initial vascular response, characterized by vasodilation and increased permeability of blood vessels, which facilitates the delivery of plasma proteins and immune cells to the affected site. This is rapidly followed by a neutrophil-dominated cellular infiltration, where polymorphonuclear leukocytes (neutrophils) are the predominant cells recruited via chemotactic signals like cytokines and chemokines; these cells engulf and destroy pathogens through phagocytosis and release of antimicrobial substances.^[18]^[1] If successful, acute inflammation progresses to a resolution phase involving the clearance of cellular debris and apoptotic neutrophils primarily through macrophage-mediated efferocytosis, alongside the downregulation of pro-inflammatory mediators to restore tissue homeostasis. Specialized pro-resolving mediators, such as resolvins derived from omega-3 fatty acids, actively promote this phase by enhancing phagocytosis and shifting macrophages toward a reparative phenotype.^[33]^[1] Common examples include the inflammatory response in wound healing, where acute inflammation aids in debris removal and epithelial regeneration; acute appendicitis, marked by neutrophil accumulation in the appendix wall; and bacterial pneumonia, involving rapid neutrophil influx into the alveoli to combat infection. These responses often manifest with the classic cardinal signs of redness, heat, swelling, pain, and loss of function, particularly in superficial tissues.^[1]^[18]

Chronic Inflammation

Chronic inflammation represents a prolonged inflammatory response that persists for months to years, distinguishing it from the shorter duration of acute inflammation. This sustained state arises primarily from persistent stimuli, such as microbial infections (e.g., Mycobacterium tuberculosis), or from inadequate resolution of initial inflammatory triggers, including autoimmune reactions or exposure to non-degradable substances.^[3] The failure of resolution mechanisms, such as impaired clearance of pathogens or dysregulated immune signaling, perpetuates the inflammatory environment, leading to ongoing tissue injury and attempted repair.^[3] Unlike acute inflammation, which relies on innate immune effectors, chronic inflammation involves adaptive immune elements that contribute to its longevity and tissue-altering effects.^[34] A hallmark of chronic inflammation is the shift in cellular infiltrates toward mononuclear cells, predominantly macrophages and lymphocytes, which replace the neutrophils dominant in acute phases. Macrophages, activated by persistent antigens, release pro-inflammatory cytokines like tumor necrosis factor-alpha (TNF-α) and interleukin-1 (IL-1), sustaining leukocyte recruitment and amplifying the response.^[3] Lymphocytes, including T cells, further orchestrate this process through antigen-specific activation, promoting the differentiation of macrophages into epithelioid cells or multinucleated giant cells. This cellular composition drives the formation of granulomas—organized aggregates of macrophages and lymphocytes that wall off indigestible material, as seen in tuberculosis where they contain mycobacteria—or excessive extracellular matrix (ECM) deposition leading to fibrosis.^[3]^[35] Tissue remodeling in chronic inflammation encompasses angiogenesis, scarring, and progressive organ dysfunction, reflecting the balance between destructive inflammation and reparative processes. New blood vessel formation, stimulated by cytokines such as vascular endothelial growth factor (VEGF) from macrophages, supplies nutrients to the inflamed site but also facilitates further immune cell infiltration.^[36] Over time, activated fibroblasts produce excessive collagen and other ECM components, resulting in fibrosis and scar tissue that replaces normal parenchyma, potentially impairing function— for instance, leading to cirrhosis in chronic hepatitis through portal tract fibrosis. In atherosclerosis, chronic inflammation promotes plaque buildup via mononuclear cell accumulation and ECM remodeling in arterial walls, while in rheumatoid arthritis, it manifests as synovial proliferation and pannus formation. Granulomatous patterns, such as those in tuberculosis, exemplify organized remodeling efforts to isolate pathogens.^[3]^[34]^[3]

Pathophysiology

Vascular Component

The vascular component of inflammation involves a series of hemodynamic alterations in the microvasculature that facilitate the delivery of plasma proteins, fluid, and immune mediators to the site of injury or infection. These changes are initiated rapidly following tissue damage or pathogen recognition, primarily through the release of local mediators that act on endothelial cells and vascular smooth muscle. The key vascular responses include vasodilation, increased permeability, and blood flow stasis, which collectively contribute to the cardinal signs of inflammation such as redness (rubor), heat (calor), and swelling (tumor).^[37] Vasodilation, the widening of arterioles and capillaries, is a primary early event that increases blood flow to the inflamed area, enhancing the supply of oxygen, nutrients, and inflammatory mediators while causing the observed erythema and warmth. This process is mediated by several key chemical signals: histamine, released from mast cells and basophils, binds to H1 receptors on endothelial cells to trigger relaxation of vascular smooth muscle; nitric oxide (NO), produced by endothelial nitric oxide synthase in response to shear stress or mediators like bradykinin, diffuses to smooth muscle cells to induce cyclic GMP-dependent relaxation; and prostaglandins, particularly PGE2 synthesized via cyclooxygenase pathways in activated cells, potentiate these effects by sensitizing vessels to other vasodilators. These mediators act synergistically, with histamine and NO often providing the initial rapid response within minutes, while prostaglandins sustain the dilation over hours.^[38]^[39]^[40] Increased vascular permeability follows vasodilation and is essential for allowing plasma components to escape into the extravascular space, forming the basis for tissue swelling. Inflammatory mediators such as histamine, leukotrienes, and cytokines induce transient contraction of endothelial cells, particularly in postcapillary venules, leading to the formation of intercellular gaps typically 0.1–0.5 μm in diameter. These gaps disrupt the endothelial barrier's tight junctions and adherens junctions, enabling the leakage of plasma proteins (e.g., fibrinogen and immunoglobulins) and fluid, which increases interstitial osmotic pressure and drives edema formation. This permeability change is reversible in acute inflammation but can become prolonged in chronic settings due to cytoskeletal remodeling. The process is tightly regulated to prevent excessive leakage, with endothelial glycocalyx and junctional proteins like VE-cadherin playing protective roles.^[41]^[42]^[43] As inflammation progresses, the influx of protein-rich plasma into tissues raises the viscosity of blood in the microvasculature, resulting in stasis or slowed blood flow, particularly in venules. This hemodynamic shift occurs because the increased diameter from vasodilation combined with plasma leakage dilutes red blood cells centrally while concentrating formed elements peripherally, promoting rouleaux formation and reduced flow velocity. Stasis facilitates leukocyte margination, where white blood cells adhere to the vessel wall, setting the stage for subsequent extravasation without directly involving cellular migration mechanisms. In severe cases, prolonged stasis can contribute to local hypoxia and thrombosis, amplifying tissue damage.^[37]^[44] These vascular alterations culminate in the formation of an exudate, a protein-rich fluid that accumulates in the interstitial spaces of inflamed tissues, distinguishing inflammatory edema from the low-protein transudate seen in non-inflammatory conditions like heart failure. Exudate typically contains 3–5 g/dL of protein (compared to <1 g/dL in transudates), along with electrolytes, clotting factors, and complement components, which support fibrin deposition for microbial containment and facilitate mediator delivery. The protein leakage, driven by the permeability changes described, creates a viscous, fibrinous matrix that aids in walling off the injury site, though excessive exudate can impair tissue function by compressing structures or promoting fibrosis if unresolved.^[37]^[45]

Cellular Component

The cellular component of inflammation encompasses the recruitment, activation, and effector functions of leukocytes, which are essential for containing and eliminating injurious agents at the site of tissue damage or infection.^[46] Leukocytes, primarily neutrophils, monocytes/macrophages, and lymphocytes, migrate from the bloodstream into inflamed tissues through a tightly regulated multistep process known as extravasation.^[47] This process is facilitated by endothelial activation in response to inflammatory signals, enabling leukocyte-endothelium interactions.^[48] Leukocyte extravasation begins with margination, where circulating leukocytes are displaced from the central flow of blood toward the vessel wall due to slowed blood flow in postcapillary venules.^[49] This is followed by rolling, a reversible tethering of leukocytes along the endothelium mediated by selectins—P-selectin and E-selectin expressed on activated endothelial cells, and L-selectin on leukocytes—which bind carbohydrate ligands such as sialyl Lewis X.^[46] Firm adhesion then occurs as chemokines presented on the endothelial surface activate leukocyte integrins (e.g., LFA-1 and Mac-1), leading to high-affinity binding to endothelial intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1).^[47] Finally, transmigration, or diapedesis, allows leukocytes to squeeze through endothelial junctions or, less commonly, via a transcellular route, guided by PECAM-1 and CD99 interactions, to enter the interstitial space.^[48] Once at the inflammatory site, leukocytes execute key effector functions, including phagocytosis, whereby neutrophils and macrophages engulf and destroy pathogens, apoptotic cells, and debris.^[50] Phagocytosis is enhanced by opsonization, in which antibodies (IgG) and complement proteins (e.g., C3b) coat targets to facilitate recognition via Fcγ receptors and complement receptors on phagocytes.^[51] Neutrophils, as rapid responders, perform efficient phagocytosis of opsonized bacteria, releasing antimicrobial granules and reactive oxygen species to kill engulfed material.^[52] Activated leukocytes further amplify the inflammatory response by secreting cell-derived mediators.^[38] Cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1), produced mainly by macrophages, promote endothelial activation, fever, and further leukocyte recruitment.^[53] Chemokines, including IL-8, direct leukocyte chemotaxis to the site, while lipid mediators like leukotrienes (e.g., LTB4) enhance vascular permeability and stimulate phagocytosis.^[54] The composition of infiltrating cells differs between acute and chronic inflammation. In acute inflammation, neutrophils predominate in the early phase (within hours), providing rapid antimicrobial defense before undergoing apoptosis.^[18] Macrophages arrive later, phagocytosing apoptotic neutrophils and transitioning the response toward resolution.^[55] In chronic inflammation, which persists beyond days to weeks, macrophages become the dominant cell type, alongside lymphocytes, sustaining tissue remodeling and fibrosis through persistent mediator release.^[56]

Clinical and Morphologic Features

Cardinal Signs and Symptoms

The cardinal signs of inflammation, originally described by the Roman encyclopedist Aulus Cornelius Celsus around 25 AD, comprise four local manifestations: redness (rubor), heat (calor), swelling (tumor), and pain (dolor).^[57] These signs arise from the vascular and cellular responses to injury or infection, providing clinicians with observable indicators of the inflammatory process. Traditionally attributed to the physician Galen in the 2nd century AD, though modern scholarship suggests it may have been added later by figures such as Rudolf Virchow in the 19th century, a fifth sign, loss of function (functio laesa), emphasizes the impairment in tissue utility due to the combined effects of pain and mechanical disruption from swelling.^[58] Redness results from vasodilation of arterioles and capillaries, which increases blood flow to the affected area and causes hyperemia.^[18] Heat stems from this enhanced perfusion, delivering warmer arterial blood and elevating local temperature, particularly noticeable in peripheral tissues.^[59] Swelling occurs due to increased vascular permeability, allowing plasma proteins and fluid to leak into the interstitial space, forming edema that distends tissues.^[18] Pain arises from the release of chemical mediators such as bradykinin and prostaglandin E2 (PGE2), which directly stimulate nociceptors or sensitize them to mechanical and thermal stimuli.^[60]^[40] Loss of function follows as a consequence of pain, edema-induced pressure on nerves and tissues, and stiffness, limiting movement or organ performance.^[6] In addition to these local signs, inflammation often produces systemic symptoms. Fever develops when endogenous pyrogens like interleukin-1 (IL-1) act on the hypothalamus, resetting the body's thermoregulatory set point and triggering heat conservation mechanisms.^[61] Malaise, characterized by fatigue and general discomfort, results from the central actions of proinflammatory cytokines such as IL-1 and IL-6, which induce behavioral changes akin to sickness behavior.^[62] Local signs like pain and swelling predominate at the site of injury, whereas systemic effects such as fever reflect broader cytokine-mediated responses.^[18] Assessment of these signs relies primarily on clinical observation, including palpation for warmth and tenderness, visual inspection for redness and swelling, and patient reports of pain and functional impairment.^[18] Imaging modalities, such as magnetic resonance imaging (MRI), can confirm edema by detecting fluid accumulation in tissues, aiding in cases where clinical signs are subtle.^[63]

Morphologic Patterns

Morphologic patterns of inflammation refer to the distinct histologic appearances observed in inflamed tissues, primarily determined by the nature and quantity of the exudate as well as the predominant cellular infiltrates. These patterns provide insights into the underlying pathologic processes and help in classifying the type and severity of the inflammatory response. They are identified through microscopic examination of tissue samples and are crucial for differentiating acute from more persistent forms of inflammation.^[64] Serous inflammation is characterized by the accumulation of a thin, watery exudate composed mainly of serum-like fluid with few cells, resulting from mild vascular permeability changes. This pattern is commonly seen in serosal cavities or skin surfaces, such as the formation of blisters in second-degree burns where the exudate separates the epidermis from the dermis. Histologically, it appears as clear, protein-poor fluid without significant cellular components.^[64] Fibrinous inflammation involves the deposition of a thick, eosinophilic exudate rich in fibrin due to extensive vascular leakage and activation of the coagulation cascade. It typically occurs on serosal surfaces, as in fibrinous pericarditis associated with rheumatic fever, where the fibrin forms a shaggy layer over the affected tissue. Under the microscope, the fibrin appears as pink, thread-like strands that may organize into fibrous tissue if the inflammation persists.^[64] Suppurative or purulent inflammation is marked by the production of pus, an exudate consisting of neutrophils, necrotic debris, and edema fluid, often triggered by pyogenic bacterial infections. This pattern manifests as localized collections like abscesses, where a central zone of liquefactive necrosis is surrounded by a wall of neutrophils and fibroblasts. Histologic examination reveals dense neutrophilic infiltrates with karyorrhectic debris, distinguishing it from other exudate types.^[64] Granulomatous inflammation features organized aggregates of macrophages, often termed granulomas, formed in response to persistent antigens that resist phagocytosis, representing a chronic inflammatory pattern. These collections include epithelioid histiocytes with elongated nuclei and abundant eosinophilic cytoplasm, sometimes fused into multinucleated giant cells, as seen in tuberculosis where central caseous necrosis may be present. Microscopically, the granulomas are compact, with surrounding lymphocytes, and lack the acute neutrophilic response of suppurative patterns.^[65] Ulcerative inflammation describes the pattern where inflammation leads to the sloughing of necrotic tissue, creating a local defect or crater on skin or mucosal surfaces due to deep tissue destruction. This occurs in areas of chronic irritation, resulting in a base of granulation tissue covered by fibrinopurulent exudate. Histologically, it shows full-thickness epithelial loss with underlying inflammation and fibrosis.^[64] The identification of these morphologic patterns relies on diagnostic tools such as tissue biopsy, which provides samples for histologic analysis, and light microscopy with special stains to highlight specific features like fibrin or microbial elements. These methods allow pathologists to correlate the observed patterns with clinical contexts, aiding in accurate diagnosis.^[64]

Systemic Effects

Acute-Phase Response

The acute-phase response represents a systemic reaction to inflammation, characterized by liver-mediated alterations in the synthesis of plasma proteins and metabolic shifts that support host defense and tissue repair. Primarily orchestrated by hepatocytes, this response involves the rapid production or suppression of specific proteins in circulation, driven by pro-inflammatory cytokines such as interleukin-6 (IL-6).^[66]^[67] Positive acute-phase proteins, whose serum concentrations increase by at least 25% during inflammation, include C-reactive protein (CRP), serum amyloid A (SAA), and fibrinogen. These proteins are transcriptionally upregulated in the liver predominantly by IL-6 signaling through pathways like STAT3 and NF-κB. CRP levels can rise dramatically, up to 1000-fold, within hours of an inflammatory stimulus.^[66]^[67] SAA, another major acute-phase reactant in humans, similarly elevates to modulate immune responses. Fibrinogen synthesis also surges to facilitate hemostasis and repair processes.^[67]^[66] Key functions of these proteins enhance innate immunity and limit infection spread. CRP acts as an opsonin by binding to phosphocholine on bacterial surfaces, promoting phagocytosis by macrophages and neutrophils while activating the complement system. SAA contributes by opsonizing gram-negative bacteria and influencing macrophage polarization toward anti-inflammatory phenotypes. Fibrinogen supports clotting to contain tissue damage and forms a provisional matrix that aids endothelial repair and leukocyte migration at injury sites.^[67]^[66] In contrast, negative acute-phase proteins, such as albumin and transferrin, exhibit decreased hepatic production to redirect metabolic resources toward defense mechanisms. Albumin levels decline to conserve amino acids for synthesizing positive acute-phase proteins, while transferrin reduction helps sequester iron from pathogens, contributing to nutritional immunity. These changes reflect a broader metabolic reprogramming in the liver during inflammation.^[67]^[66] CRP serves as a sensitive biomarker for assessing inflammation intensity, with serum levels exceeding 10 mg/L typically signaling an acute response. This threshold distinguishes acute inflammation from baseline states (normal range: <10 mg/L) and aids in monitoring conditions like infections or tissue injury.^[66]

Hematologic Changes

Inflammation induces significant alterations in peripheral blood cell populations, primarily through cytokine-mediated signaling that stimulates bone marrow production and release of leukocytes. In acute inflammation, leukocytosis is a hallmark response, characterized by an elevated white blood cell count typically exceeding 11,000 cells/μL, predominantly due to neutrophilia as neutrophils are rapidly mobilized to combat infection or tissue injury.^[68] This neutrophilic predominance reflects the innate immune system's priority in containing acute threats, with cytokines such as interleukin-6 (IL-6) and granulocyte colony-stimulating factor (G-CSF) driving granulopoiesis and demargination of neutrophils from vascular pools.^[69] In contrast, chronic inflammation often features lymphocytosis, with absolute lymphocyte counts surpassing 4,000 cells/μL, arising from persistent antigenic stimulation that promotes lymphocyte proliferation and recruitment, as seen in conditions like autoimmune diseases or chronic infections.^[70]^[71] Thrombocytosis, or elevated platelet counts above 450,000/μL, commonly accompanies both acute and chronic inflammation as a reactive process mediated by IL-6 and other proinflammatory cytokines that enhance megakaryocyte maturation in the bone marrow.^[72] This increase supports hemostasis by bolstering the availability of platelets for rapid clot formation at sites of vascular damage or endothelial activation during inflammatory states, thereby preventing excessive bleeding amid heightened tissue repair demands.^[73] While beneficial in moderation, extreme thrombocytosis can predispose to thrombotic complications if inflammation persists unchecked.^[72] The anemia of chronic disease, also known as anemia of inflammation, develops in prolonged inflammatory states through hepcidin-mediated iron sequestration, where the liver-derived peptide hepcidin inhibits ferroportin, the primary iron exporter on macrophages and enterocytes, leading to hypoferremia and restricted iron availability for erythropoiesis.^[74] Proinflammatory cytokines like IL-6 upregulate hepcidin expression, diverting iron stores into macrophages for nutritional immunity against pathogens while impairing hemoglobin synthesis, resulting in normocytic, normochromic anemia with hemoglobin levels often below 11 g/dL.^[75] This mechanism underscores inflammation's role in prioritizing host defense over red blood cell production.^[76] Inflammation also shifts the coagulation system toward a procoagulant state, primarily via upregulated expression of tissue factor (TF) on endothelial cells, monocytes, and vascular smooth muscle cells in response to cytokines such as tumor necrosis factor-alpha (TNF-α) and IL-1.^[77] TF initiates the extrinsic coagulation pathway by forming a complex with factor VIIa, accelerating thrombin generation and fibrin deposition to localize hemostasis at inflammatory foci.^[78] This interplay between inflammation and coagulation, often termed thromboinflammation, enhances barrier integrity but risks disseminated intravascular coagulation if dysregulated.^[77]

Role in Disease

Contribution to Chronic Diseases

Chronic inflammation, characterized by persistent activation of immune responses without effective resolution, plays a pivotal role in the pathogenesis and progression of various non-communicable diseases by promoting tissue damage, fibrosis, and dysfunction.^[79] In these conditions, unresolved inflammatory signals amplify cellular stress, leading to maladaptive remodeling and heightened risk of complications.^[80] In atherosclerosis, low-density lipoprotein (LDL) oxidation triggers endothelial dysfunction, initiating a cascade of inflammatory events that culminate in plaque formation and instability. Oxidized LDL (oxLDL) binds to scavenger receptors on endothelial cells, upregulating adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1), which facilitate monocyte recruitment and infiltration into the subendothelial space.^[81] These monocytes differentiate into macrophages that engulf oxLDL, forming foam cells and releasing pro-inflammatory cytokines like interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), which perpetuate endothelial injury and smooth muscle cell proliferation.^[79] This chronic inflammatory milieu within plaques contributes to their rupture, thrombosis, and acute cardiovascular events such as myocardial infarction.^[82] Autoimmune disorders exemplify how dysregulated inflammation drives targeted tissue destruction. In rheumatoid arthritis (RA), synovial inflammation leads to hyperplasia of the synovial lining, characterized by proliferation of fibroblast-like synoviocytes and influx of immune cells, forming an invasive pannus that erodes cartilage and bone.^[83] Cytokines such as TNF-α and IL-6, produced by activated macrophages and T cells in the synovium, sustain this hyperplasia and angiogenesis, amplifying joint destruction.^[84] Similarly, in type 1 diabetes, autoimmune-mediated inflammation targets pancreatic β-cells, resulting in their progressive destruction through mechanisms involving T-cell infiltration and cytokine-induced apoptosis. Pro-inflammatory cytokines like interferon-γ (IFN-γ) and IL-1β impair β-cell function and survival, leading to insulin deficiency and hyperglycemia.^[85] This inflammatory assault, often initiated by viral triggers or genetic susceptibility, culminates in near-complete β-cell loss.^[86] Metabolic syndrome involves adipose tissue inflammation as a central driver of insulin resistance, particularly in obesity. Hypertrophic adipocytes in obese individuals secrete chemokines like monocyte chemoattractant protein-1 (MCP-1), recruiting macrophages that polarize toward a pro-inflammatory M1 phenotype and release TNF-α and IL-6.^[80] This chronic low-grade inflammation impairs insulin signaling by activating pathways such as c-Jun N-terminal kinase (JNK) and nuclear factor-κB (NF-κB), which serine-phosphorylate insulin receptor substrate-1 (IRS-1), reducing glucose uptake in adipose and peripheral tissues.^[87] Consequently, systemic insulin resistance ensues, linking adipose inflammation to metabolic dysregulation and increased risk of type 2 diabetes and cardiovascular disease.^[80] Neuroinflammation contributes to neurodegeneration in Alzheimer's disease through microglial activation, which exacerbates amyloid-β plaque buildup and tau pathology. Activated microglia, triggered by amyloid-β aggregates, release pro-inflammatory mediators like IL-1β and TNF-α, promoting a vicious cycle of neuronal injury and tau hyperphosphorylation. Recent research highlights how this microglial response, involving TREM2 signaling dysregulation, facilitates tau propagation across brain regions, accelerating cognitive decline.^[88] In the 2020s, studies have emphasized tau's role in sustaining microglial activation, independent of amyloid, underscoring neuroinflammation's centrality in disease progression.^[89]

Inflammation in Cancer and Immunity

Inflammation plays a dual role in cancer, acting both as a promoter of tumor development and as a facilitator of anti-tumor immune responses. Chronic inflammation is recognized as a key enabling characteristic of cancer, often described as the "seventh hallmark" alongside the original six biological capabilities acquired by tumor cells, such as sustaining proliferative signaling and evading growth suppressors.^[90] This perspective was updated in subsequent analyses, emphasizing how persistent inflammatory processes contribute to tumor microenvironment (TME) reprogramming that supports neoplastic progression.^[91] In contrast, acute inflammatory responses can enhance immunosurveillance by recruiting and activating immune effectors like natural killer (NK) cells and cytotoxic T cells, which directly target and eliminate nascent tumor cells through mechanisms including perforin-mediated lysis and cytokine release.^[92] Pro-tumorigenic effects of inflammation are mediated primarily by proinflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), which foster angiogenesis, extracellular matrix remodeling, and metastatic dissemination. IL-6, secreted by tumor-associated macrophages and cancer cells, activates the JAK/STAT3 pathway in endothelial cells to upregulate vascular endothelial growth factor (VEGF), thereby promoting neovascularization essential for tumor growth and invasion.^[93] Similarly, TNF-α enhances epithelial-to-mesenchymal transition (EMT) in cancer cells, increasing their migratory potential and resistance to apoptosis, while also recruiting myeloid-derived suppressor cells that dampen adaptive immunity.^[94] These cytokine-driven processes exemplify how chronic inflammation sustains a permissive TME, as seen in infections like Helicobacter pylori, where persistent gastric mucosal inflammation induces oxidative stress, DNA damage, and progression to adenocarcinoma through activation of NF-κB signaling.^[95] Another illustrative case is colitis-associated colorectal cancer (CAC), in which inflammatory bowel disease leads to repeated cycles of epithelial injury and repair, elevating risk via IL-6-mediated STAT3 activation and prostaglandin E2 production that drive dysplasia and invasion.^[96] On the protective side, acute inflammation bolsters anti-tumor immunity by initiating the recruitment of NK cells, which recognize stress ligands on transformed cells (e.g., MICA/MICB) and produce interferon-gamma (IFN-γ) to amplify T-cell responses.^[97] This coordinated action helps clear immunogenic tumors, particularly when inflammation is triggered by therapies like chemotherapy that expose damage-associated molecular patterns (DAMPs). Recent advances in the 2020s have leveraged this inflammatory-immune axis through PD-1 checkpoint inhibitors, such as pembrolizumab and nivolumab, which reinvigorate exhausted T cells in the TME, enhancing cytotoxic activity against solid tumors like melanoma and non-small cell lung cancer.^[98] These immunotherapies harness endogenous inflammatory cues to overcome tumor immune evasion, achieving durable responses in approximately 20-40% of patients across indications, though combination strategies with cytokine modulators are under investigation to mitigate chronic pro-tumor biases.^[99]

Resolution and Outcomes

Mechanisms of Resolution

The resolution of inflammation is an active, programmed process that actively terminates inflammatory responses and restores tissue homeostasis, rather than a passive dissipation of signals. This phase involves the orchestrated action of specialized pro-resolving mediators (SPMs), cellular clearance mechanisms, and regulatory immune cells to limit leukocyte recruitment, promote debris removal, and facilitate repair without immunosuppression.^[100] SPMs, including lipoxins derived from the ω-6 polyunsaturated fatty acid (PUFA) arachidonic acid and resolvins, protectins, and maresins from ω-3 PUFAs such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), play a central role by countering pro-inflammatory eicosanoids like leukotrienes and prostaglandins. These mediators are biosynthesized via enzymatic pathways involving cyclooxygenases and lipoxygenases during the transition from initiation to resolution phases of inflammation. For instance, lipoxin A4 inhibits neutrophil transmigration and stimulates macrophage phagocytosis, while resolvins (e.g., resolvin D1) and protectins (e.g., protectin D1) reduce cytokine production (such as TNF-α and IL-6) and enhance antimicrobial actions without compromising host defense. By binding to specific G-protein-coupled receptors like ALX/FPR2 and GPR32, SPMs promote the "switch" from pro-inflammatory to pro-resolving signals, ensuring timely clearance of exudates and apoptotic cells.^[100]00077-6) Efferocytosis, the phagocytic removal of apoptotic cells by macrophages, is a key non-inflammatory clearance mechanism that prevents secondary necrosis and the release of damage-associated molecular patterns, thereby dampening further inflammation. Macrophages recognize apoptotic cells through "eat-me" signals like exposed phosphatidylserine via receptors such as TIM-4 and MerTK, leading to engulfment without triggering pro-inflammatory responses; instead, it induces anti-inflammatory cytokine production (e.g., IL-10, TGF-β) and metabolic reprogramming for tissue repair. This process is essential for resolving acute inflammation, as defects in efferocytosis impair resolution and contribute to persistent inflammation.^[101]00527-1) Regulatory T cells (Tregs), particularly Foxp3+ CD4+ Tregs, suppress effector T cell and innate immune responses to facilitate resolution, primarily through secretion of immunosuppressive cytokines like IL-10 and TGF-β. IL-10 from Tregs inhibits pro-inflammatory cytokine release from macrophages and dendritic cells, while TGF-β promotes wound healing and immune tolerance by downregulating NF-κB signaling in effector cells. These actions are context-specific, often at mucosal barriers, and are critical for preventing excessive immune activation during resolution.^[102]30335-2) Failure of these resolution mechanisms, such as insufficient SPM production or impaired efferocytosis, can lead to non-resolving inflammation and chronicity, as seen in conditions like atherosclerosis where persistent apoptotic cell accumulation drives disease progression. Recent post-2020 research has advanced SPMs toward clinical application; for example, a 2023 randomized controlled trial demonstrated that SPM-enriched fish oil supplementation reduced pain in osteoarthritis patients, highlighting potential therapeutic translation for resolving chronic inflammation.^[101]^[103]

Potential Complications

Prolonged or dysregulated inflammation can lead to fibrosis and scarring through excessive deposition of extracellular matrix components, particularly collagen, in affected tissues. This process often follows unresolved acute inflammatory responses, where persistent activation of fibroblasts and myofibroblasts results in the replacement of normal parenchymal tissue with fibrotic scar tissue, impairing organ function. A prominent example is pulmonary fibrosis developing after acute respiratory distress syndrome (ARDS), where initial alveolar injury triggers ongoing inflammation that evolves into widespread lung scarring, reducing gas exchange capacity and leading to chronic respiratory failure.^[104]^[105] Inflammation can escalate from a localized protective response to systemic autoimmunity, particularly in genetically susceptible individuals, by promoting the breakdown of immune tolerance and the production of autoantibodies. This progression involves chronic immune activation that exposes self-antigens, leading to autoreactive B- and T-cell responses and tissue damage. For instance, initial inflammatory triggers may contribute to the development of systemic lupus erythematosus (SLE), a multisystem autoimmune disorder characterized by widespread inflammation in organs such as the kidneys, skin, and joints due to immune complex deposition.^[106]^[107] Overactivation of the inflammatory cascade in response to infection or injury can precipitate sepsis, defined as a life-threatening organ dysfunction caused by a dysregulated host response. This manifests as systemic inflammatory response syndrome (SIRS), involving widespread endothelial dysfunction, microvascular leakage, and coagulopathy, which can rapidly progress to septic shock and multi-organ failure. Diagnostic criteria for sepsis have evolved, with the Sequential Organ Failure Assessment (SOFA) score—updated in recent guidelines—used to quantify organ dysfunction, where a change of 2 or more points indicates high mortality risk, emphasizing the need for early recognition of inflammatory overdrive.^[108]^[109]^[110] Inflammaging refers to the chronic, low-grade systemic inflammation that accumulates with advancing age, driven by cellular senescence and the senescence-associated secretory phenotype (SASP), which perpetuates a pro-inflammatory milieu. This state contributes to age-related frailty by exacerbating muscle loss, metabolic dysregulation, and immune exhaustion, increasing vulnerability to infections and comorbidities. Recent studies have expanded on this concept, linking inflammaging to senescent cell accumulation in tissues, which amplifies inflammatory signaling pathways like NF-κB, thereby accelerating physiological decline in older adults.^[111]^[112]^[113] Chronic inflammation also heightens the risk of cancer by fostering a tumor-promoting microenvironment, though this is explored in detail under inflammation's role in oncology.^[114]

Treatment Approaches

Pharmacologic Interventions

Pharmacologic interventions for inflammation primarily target key molecular pathways to suppress excessive immune responses, with classes including corticosteroids, nonsteroidal anti-inflammatory drugs (NSAIDs), biologics, and agents for allergic inflammation. These therapies modulate cytokine production, enzyme activity, and cellular signaling to alleviate symptoms and prevent tissue damage in acute and chronic conditions. Selection depends on the inflammatory type, severity, and patient factors, often guided by clinical guidelines from bodies like the American College of Rheumatology. Corticosteroids, particularly glucocorticoids such as prednisone, exert broad anti-inflammatory effects by binding to glucocorticoid receptors, which translocate to the nucleus and inhibit pro-inflammatory transcription factors like NF-κB through induction of inhibitory proteins such as IκBα. This mechanism suppresses the expression of multiple inflammatory mediators, including cytokines (e.g., IL-1, IL-6), chemokines, and adhesion molecules, providing rapid symptom relief in conditions like rheumatoid arthritis and asthma exacerbations. Long-term use requires monitoring for side effects like osteoporosis due to their potent but non-specific suppression. Nonsteroidal anti-inflammatory drugs (NSAIDs), exemplified by ibuprofen, inhibit cyclooxygenase (COX) enzymes—primarily COX-1 and COX-2—to block the conversion of arachidonic acid into prostaglandins, key mediators of pain, fever, and inflammation in acute settings such as osteoarthritis or post-surgical recovery. By reducing prostaglandin synthesis, NSAIDs decrease vascular permeability and leukocyte recruitment at inflammation sites, though selective COX-2 inhibitors like celecoxib minimize gastrointestinal risks associated with non-selective agents. Biologic therapies target specific cytokines in autoimmune-driven inflammation; anti-tumor necrosis factor (TNF) agents like infliximab, a monoclonal antibody, neutralize soluble and membrane-bound TNF-α, preventing its binding to receptors and downstream activation of inflammatory cascades in diseases such as Crohn's disease and psoriasis. These agents induce apoptosis in TNF-expressing cells and reduce levels of other cytokines like IL-6 and IL-12, leading to sustained remission in many patients. Recent advancements include IL-23 inhibitors, with mirikizumab approved by the FDA in 2023 for ulcerative colitis and in 2025 for Crohn's disease, selectively blocking the IL-23/IL-17 axis to curb Th17-mediated inflammation without broadly impairing immunity. For allergic inflammation, antihistamines such as diphenhydramine competitively antagonize H1 histamine receptors on endothelial and smooth muscle cells, mitigating vasodilation, bronchoconstriction, and itching in conditions like urticaria or allergic rhinitis. Mast cell stabilizers, including cromolyn sodium, inhibit calcium influx into mast cells to prevent degranulation and release of histamine, leukotrienes, and other mediators, offering prophylactic benefits in asthma and conjunctivitis by stabilizing cell membranes during allergen exposure.

Non-Pharmacologic Strategies

Non-pharmacologic strategies for managing inflammation emphasize lifestyle modifications that target underlying contributors such as oxidative stress, immune dysregulation, and metabolic factors, often yielding reductions in circulating inflammatory markers like C-reactive protein (CRP) and interleukin-6 (IL-6). These approaches are supported by clinical evidence showing benefits in preventing or alleviating chronic low-grade inflammation associated with conditions like cardiovascular disease and metabolic syndrome.^[115]^[116] Dietary interventions form a cornerstone, with anti-inflammatory diets promoting whole, plant-based foods rich in polyphenols, fiber, and omega-3 fatty acids while limiting processed sugars and trans fats. The Mediterranean diet, characterized by high intake of fruits, vegetables, whole grains, nuts, legumes, and fatty fish, has been shown to reduce CRP levels by up to 20% and lower cardiovascular event risk by 30% in high-risk populations. Similarly, the DASH diet, emphasizing fruits, vegetables, low-fat dairy, and reduced sodium, decreases inflammatory biomarkers and supports blood pressure control, thereby mitigating vascular inflammation. High-fiber plant-based diets enhance gut microbiota diversity, increasing short-chain fatty acid production that suppresses pro-inflammatory pathways.^[117]^[117]^[118] Regular physical activity, including aerobic and resistance training, induces anti-inflammatory effects by modulating cytokine production and improving insulin sensitivity. Moderate-intensity exercise, such as brisk walking for 30 minutes daily, reduces systemic inflammation markers like IL-6 and tumor necrosis factor-alpha (TNF-α) in older adults and those with metabolic syndrome, with meta-analyses confirming a 10-15% decrease in CRP after consistent training. Resistance training further lowers low-grade inflammation linked to type 2 diabetes and cardiovascular disease, though excessive high-intensity exercise may transiently elevate markers, underscoring the importance of moderation. Combining exercise with dietary changes amplifies benefits, as seen in interventions where lifestyle programs reduced inflammation more effectively than diet or exercise alone.^[119]^[120]^[121] Adequate sleep duration and quality are essential, as chronic sleep deprivation elevates pro-inflammatory cytokines including IL-6 and CRP, contributing to heightened immune activation. Adults achieving 7-9 hours of restorative sleep nightly exhibit lower inflammation levels, with experimental studies demonstrating that even partial sleep restriction increases inflammatory responses within days. Interventions improving sleep hygiene, such as consistent bedtime routines, have been linked to reduced CRP in populations with insomnia, highlighting sleep's role in immune homeostasis.^[122]^[123]^[124] Stress management techniques, including mindfulness meditation, yoga, and deep breathing, counteract the pro-inflammatory effects of chronic psychological stress, which activates the hypothalamic-pituitary-adrenal axis and elevates cortisol and cytokines. Mind-body practices like yoga reduce TNF-α and IL-6 by 10-20% in randomized trials, particularly in individuals with chronic inflammatory conditions, by enhancing parasympathetic activity and resilience. These interventions also improve overall adherence to other lifestyle changes, fostering sustained inflammation control.^[125]^[126]^[127] Weight management through caloric restriction and sustained lifestyle changes directly addresses adipocyte-driven inflammation, as visceral fat accumulation promotes cytokine release. Intentional weight loss of 5-10% body weight via diet and exercise decreases CRP by 20-30% and improves adipose tissue inflammation in obese individuals, with bariatric surgery showing even greater reductions in systemic markers. This strategy is particularly impactful in metabolic disorders, where it interrupts the cycle of inflammation and insulin resistance.^[128]^[115]^[129]

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