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Eosinophil

Eosinophils are a type of granulocyte white blood cell characterized by a bilobed nucleus and large cytoplasmic granules that stain bright red-orange with the acidic dye eosin, from which they derive their name.^[1]^[2] They typically constitute 1–4% of circulating leukocytes in healthy adults, with absolute counts below 500 cells per microliter of blood.^[3] Produced in the bone marrow from myeloid progenitors in response to cytokines such as interleukin-5 (IL-5), interleukin-3 (IL-3), and granulocyte-macrophage colony-stimulating factor (GM-CSF), eosinophils mature over 8–12 days before entering the bloodstream, where they have a short half-life of 8–18 hours, and primarily accumulate in tissues like the gastrointestinal tract, lungs, and skin.^[4]^[5] Beyond their classic role in host defense against helminth parasites—through the release of cytotoxic granule proteins such as major basic protein (MBP), eosinophil cationic protein (ECP), eosinophil peroxidase (EPX), and eosinophil-derived neurotoxin (EDN)—eosinophils exhibit multifaceted functions in innate and adaptive immunity.^[6]^[5] These include combating bacterial and viral infections via extracellular trap formation and antimicrobial peptides, promoting tissue repair and homeostasis through growth factors and lipid mediators, and modulating allergic responses by interacting with T cells, B cells, and mast cells.^[7]^[8] In disease states, dysregulated eosinophil activation contributes to pathology in conditions like asthma, chronic rhinosinusitis with nasal polyps, eosinophilic gastrointestinal disorders, and hypereosinophilic syndromes, where elevated levels lead to tissue inflammation and damage.^[5]^[9] Emerging evidence also underscores their involvement in antitumor immunity and immunoregulation, challenging the traditional view of eosinophils solely as proinflammatory effectors.^[5]^[10]

Structure and Morphology

Physical Characteristics

Eosinophils are a type of granulocyte that measure 12 to 17 μm in diameter, making them slightly larger than neutrophils. They are readily identifiable in peripheral blood smears due to their distinctive morphology. The nucleus is typically bilobed or segmented, consisting of two lobes connected by thin chromatin strands, with densely packed and clumped chromatin that gives it a compact appearance under light microscopy. In Romanowsky stains, the nucleus stains purple, contrasting with the cytoplasm's bright coloration. The cytoplasm of eosinophils is abundant and filled with large, refractile granules that dominate its appearance. These granules, measuring 0.5 to 0.8 μm in diameter, stain intensely red or orange with eosin dye or Romanowsky methods, owing to their basic protein content, which sets eosinophils apart from other leukocytes like neutrophils and basophils. This eosinophilia is the basis for their name and primary means of identification in histological preparations. The granular cytoplasm imparts a segmented, lobulated look to the cell overall. In circulation, eosinophils exhibit a short half-life of 8–18 hours, after which they migrate to tissues where they can persist for 8 to 12 days, particularly in the respiratory and gastrointestinal tracts.^[11] At the ultrastructural level, as revealed by electron microscopy, mature eosinophils contain specific granules bounded by a trilaminar membrane; these granules often feature a central crystalloid core surrounded by an electron-lucent matrix, though some appear coreless, especially in immature forms. Variations between mature and immature eosinophils include the presence or absence of these crystalloid structures, with coreless granules more common in developing cells. These structural features underpin the cell's identification and support its roles in immune responses, such as through granule-mediated effector functions.

Cellular Markers and Receptors

Eosinophils are identified and distinguished from other leukocytes through specific surface markers that are routinely used in flow cytometry and immunohistochemical analyses. Key markers include CD9, a tetraspanin protein involved in cell activation and adhesion; CD11b, an integrin subunit that contributes to phagocytic and adhesive functions; CD15, a carbohydrate antigen associated with granulocyte differentiation; and CD44, a hyaluronan-binding adhesion molecule that aids in cell retention within tissues.^[12] These markers, along with the bilobed nucleus and granule staining, provide a biochemical profile for eosinophil enumeration in blood and tissues.^[12] In humans, Siglec-8 serves as a distinctive inhibitory receptor on eosinophils, promoting apoptosis upon ligand binding and distinguishing them from neutrophils and other granulocytes; in mice, the ortholog Siglec-F fulfills a similar role in regulating eosinophil survival and activation.^[13] Eosinophils also express receptors for immunoglobulins that mediate antibody-dependent cellular cytotoxicity and immune complex interactions. These include the high-affinity FcεRI for IgE, which facilitates allergen recognition; the inhibitory FcγRII (CD32) for IgG, which modulates activation signals; and FcαR (CD89) for IgA, enabling responses to mucosal pathogens.^[14] Chemokine and cytokine receptors on eosinophils direct their recruitment and survival in inflammatory sites. CCR1 binds various chemokines to support initial chemotaxis, while CCR3 is the primary receptor for eotaxins (such as CCL11), driving selective eosinophil accumulation in allergic responses.^[15] The IL-5Rα chain forms the high-affinity receptor for interleukin-5 (IL-5), essential for eosinophil proliferation, differentiation, and prolonged survival. Adhesion molecules further enable eosinophil interactions with the vascular endothelium and extracellular matrix. VLA-4 (integrin α4β1) binds vascular cell adhesion molecule-1 (VCAM-1) on activated endothelial cells, facilitating firm adhesion and transendothelial migration during inflammation.^[12] These receptors collectively allow eosinophils to sense and respond to chemotactic gradients, as detailed in studies of tissue migration.^[12]

Development and Maturation

Hematopoietic Origin

Eosinophils originate in the bone marrow from hematopoietic stem cells (HSCs) that differentiate through a series of committed progenitors, beginning with the common myeloid progenitor (CMP), a multipotent cell derived from the multilineage hematopoietic progenitor.^[16] This lineage commitment is tightly regulated by specific transcription factors, including GATA-binding protein 1 (GATA1), which enforces eosinophil fate by switching myeloid progenitors toward the eosinophil lineage, and CCAAT/enhancer-binding protein epsilon (C/EBPε), which promotes eosinophil-specific differentiation while repressing alternative myeloid paths like neutrophilia.^[17]^[18] GATA1 and C/EBPε act sequentially with early factors like C/EBPα to drive initial commitment from CMPs, ensuring the development of eosinophil-basophil progenitors (EBPs) as key intermediates that branch toward eosinophils or basophils.^[19] The maturation process is heavily dependent on cytokines, with interleukin-5 (IL-5) serving as the primary driver of eosinophil growth, differentiation, and survival from the progenitor stage onward.^[4] IL-5 synergizes with interleukin-3 (IL-3) and granulocyte-macrophage colony-stimulating factor (GM-CSF), which provide supportive signals for early progenitor expansion and later maturation, particularly in response to inflammatory cues.^[20] These cytokines bind to shared or specific receptors on EBPs and downstream cells, promoting proliferation while maintaining eosinophil poise over other granulocyte lineages like neutrophils. Eosinophil development progresses through distinct morphological stages in the bone marrow: starting from promyelocytes, which initiate granule formation, to myelocytes where secondary granules (eosinophil-specific) accumulate, followed by metamyelocytes, band cells, and finally mature segmented eosinophils characterized by bilobed nuclei and granule-laden cytoplasm.^[21] EBPs represent a committed intermediate stage post-CMP, where cells begin expressing eosinophil markers under cytokine influence before advancing through these granulocytic stages.^[22] Regulation of this process centers on IL-5 receptor signaling, which activates the Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway to enhance progenitor survival and terminal maturation by upregulating anti-apoptotic genes and differentiation factors.^[23] Specifically, IL-5 binding to its receptor triggers JAK2 phosphorylation, leading to STAT5 activation that sustains eosinophilopoiesis without excessive proliferation.^[24] Mature eosinophils are then released into the bloodstream for circulation or tissue recruitment.^[4]

Tissue Migration and Activation

Eosinophils egress from the bone marrow primarily through mechanisms involving sphingosine-1-phosphate (S1P) gradients and downregulation of the chemokine receptor CXCR4. The S1P-S1P1 receptor axis facilitates the release of mature eosinophils into the circulation by creating a concentration gradient that promotes their exit from the hematopoietic niche; disruption of this pathway, as seen with the S1P modulator FTY720, leads to eosinophil accumulation in the bone marrow and reduced circulating numbers.^[25] Concurrently, downregulation of CXCR4 expression diminishes retention signals from stromal cell-derived factor-1 (SDF-1/CXCL12), allowing eosinophils to leave the bone marrow, a process analogous to that in other granulocytes and observed in response to inflammatory cues like allergen exposure.03069-6/fulltext) Once in the bloodstream, eosinophils exhibit rapid chemotaxis to inflamed tissues, orchestrated by eotaxins (CCL11, CCL24, and CCL26) that bind to the G-protein-coupled receptor CCR3 on their surface. This interaction triggers a multi-step adhesion cascade: initial rolling along the vascular endothelium mediated by selectins (e.g., P-selectin and E-selectin), followed by firm adhesion via upregulated integrins such as very late antigen-4 (VLA-4/α4β1) interacting with vascular cell adhesion molecule-1 (VCAM-1), and culminating in diapedesis through the endothelial barrier.^[12] These chemokines are produced by epithelial and endothelial cells in response to type 2 cytokines, ensuring selective recruitment of eosinophils to sites of allergic or parasitic inflammation.^[12] In tissues such as the gastrointestinal tract and lungs, eosinophils establish long-term residency, contrasting their short half-life of 8–18 hours in the blood. Tissue eosinophils can persist for 36 hours in the lungs or up to 6–8 days in the intestines, supported by local survival factors that maintain their viability and functional readiness.^[26] Activation occurs upon exposure to local signals, including interleukin-5 (IL-5) from T helper 2 cells or allergens, which prolong survival and enhance effector potential without immediate degranulation.^[12] Priming of tissue-resident eosinophils involves cytokine-mediated upregulation of adhesion molecules and receptor expression, preparing them for rapid responses. Cytokines such as IL-5 and granulocyte-macrophage colony-stimulating factor (GM-CSF) increase surface expression of integrins (e.g., CD11b/CD18) and CCR3, heightening sensitivity to chemotactic gradients and facilitating further recruitment or activation.^[27] This priming state, induced by exposure to type 2 microenvironmental signals, enhances eosinophil adhesion to extracellular matrix components and responsiveness to subsequent stimuli, thereby amplifying their role in ongoing immune processes.^[12]

Physiological Roles

Defense Against Parasites

Eosinophils play a specialized role in the host's immune defense against multicellular parasites, particularly helminths, by employing targeted cytotoxic mechanisms that limit parasite viability and reproduction.^[4] These granulocytes are recruited to infection sites where they interact with parasite-bound antibodies, facilitating direct damage to the parasite's integument without relying on phagocytosis, which is ineffective against large pathogens.^[28] A primary mechanism is antibody-dependent cell-mediated cytotoxicity (ADCC), in which eosinophils bind to IgG- or IgE-coated parasites through Fc receptors on their surface, triggering the release of cytotoxic granule proteins that disrupt the parasite's membrane.^[29] This process is particularly effective against large helminths such as schistosomes and nematodes, where eosinophils deposit toxic proteins onto the parasite surface, leading to immobilization and death; however, eosinophils are less efficient against smaller pathogens like protozoa or bacteria due to their limited phagocytic capacity.^[4] Nevertheless, eosinophils contribute to antibacterial defense through extracellular trap formation and release of antimicrobial granule proteins such as eosinophil cationic protein (ECP) and eosinophil peroxidase (EPX), which exhibit bactericidal activity.^[30] In addition to granule release, eosinophils form extracellular traps (EETs) by expelling mitochondrial DNA decorated with granule proteins, which ensnare and further damage parasite larvae, as observed in filarial infections.^[31] From an evolutionary perspective, eosinophils are prominent in mammals frequently exposed to parasitic helminths, suggesting their adaptation as a key antiparasitic defense.^[32] Interleukin-5 (IL-5), produced by T helper 2 cells in response to parasitic antigens, enhances eosinophil recruitment, activation, and survival at infection sites, amplifying this protective response.^[4] Granule proteins involved in these mechanisms, such as major basic protein, are central to the cytotoxicity but are detailed in the section on major protein components.

Modulation of Allergic and Inflammatory Responses

Eosinophils play a central role in type 2 immune responses, particularly in allergic and chronic inflammatory conditions, where they are recruited to sites of allergen exposure through Th2 cytokines such as IL-4, IL-13, and IL-5. These cytokines promote eosinophil differentiation, survival, and migration into tissues like the airways and mucosa, leading to inflammation in disorders such as asthma and allergic rhinitis. For instance, IL-5 specifically enhances eosinophil activation and chemotaxis, while IL-4 and IL-13 induce endothelial expression of vascular cell adhesion molecule-1 (VCAM-1) and chemokines like eotaxin (CCL11), facilitating eosinophil adhesion and infiltration.^[33]^[34]^[35] In their pro-inflammatory capacity, eosinophils exacerbate allergic and inflammatory responses by releasing a variety of mediators, including cytokines like IL-6 and TGF-β, as well as lipid mediators such as leukotrienes. These molecules drive mucus hypersecretion from goblet cells, smooth muscle contraction, and fibroblast activation, contributing to airway hyperresponsiveness and tissue remodeling. TGF-β, in particular, stimulates collagen deposition and extracellular matrix production, promoting fibrosis in chronic settings. Leukotrienes like LTC4 further amplify vascular permeability and bronchoconstriction, intensifying local inflammation.^[33]^[34]^[35] Eosinophils exhibit a dual role in modulating allergic and inflammatory responses, acting both as effectors that worsen pathology through degranulation and as regulators that dampen excessive immunity. In pro-inflammatory actions, their granular proteins and mediators sustain type 2 inflammation, while in regulatory functions, eosinophils induce apoptosis in activated T cells via indoleamine 2,3-dioxygenase (IDO) expression, thereby limiting T-cell proliferation and cytokine production in chronic environments. Additionally, eosinophils promote tissue repair and homeostasis by secreting growth factors such as vascular endothelial growth factor (VEGF) and transforming growth factor-β (TGF-β) in reparative contexts, as well as lipid mediators like resolvin E1, which facilitate wound healing and inflammation resolution.^[33]^[35]^[36]^[4]^[37] This balance helps prevent uncontrolled tissue damage during prolonged inflammation.^[33]^[35]^[36] Beyond allergy, eosinophils contribute modestly to antiviral defense within type 2 contexts by producing IFN-γ and serving as antigen-presenting cells through MHC class II expression. Activated eosinophils upregulate MHC II and costimulatory molecules like CD80, enabling them to present viral antigens to CD4+ T cells and promote IFN-γ secretion, which aids in limiting viral replication in mucosal tissues. However, this role remains limited compared to their dominant functions in allergic inflammation.^[33]^[36]

Granule Contents and Mechanisms

Major Protein Components

Eosinophils store a variety of cytotoxic and enzymatic proteins within their secondary (specific) granules, primarily in the crystalloid core and matrix, which contribute to their roles in innate immunity. These major protein components include major basic protein (MBP), eosinophil cationic protein (ECP), eosinophil-derived neurotoxin (EDN), eosinophil peroxidase (EPO), and Charcot-Leyden crystal protein (CLC, also known as galectin-10). Each exhibits distinct biochemical properties, such as high cationic charge or enzymatic activity, enabling them to target pathogens and modulate cellular responses upon release. Major basic protein (MBP), the most abundant granule constituent at approximately 50% of total granule protein by mass, is a small, highly cationic molecule with a molecular weight of about 14 kDa. Rich in arginine residues, MBP carries a strong positive charge (pI ≈ 11.4), allowing it to bind and disrupt lipid bilayers of parasite membranes, mammalian cells, and bacteria through non-enzymatic mechanisms. This arginine-rich structure facilitates its polymerization and toxicity, contributing to helminth killing and potential tissue damage in inflammatory settings.^[38]^[39] Eosinophil cationic protein (ECP), a member of the ribonuclease A superfamily with a molecular weight of approximately 18 kDa, possesses potent ribonuclease activity and a high cationic charge (pI ≈ 10.8). Its neurotoxic effects stem from RNA degradation, while its antiviral properties arise from disrupting viral envelopes and inhibiting replication; additionally, ECP induces histamine release from basophils, amplifying allergic responses. Glycosylation variants contribute to its molecular heterogeneity, enhancing its stability and broad-spectrum antimicrobial action against bacteria, viruses, and helminths.^[39]^[40] Closely related to ECP, eosinophil-derived neurotoxin (EDN) is another 18 kDa ribonuclease A family member (pI ≈ 8.9) with strong ribonucleolytic activity but lower cationic charge. EDN exhibits neurotoxicity, famously inducing the Gordon phenomenon—a syndrome of ataxia and paralysis—in rabbits and mice via intracerebral injection, due to selective damage to central nervous system white matter. It also demonstrates antiviral effects by degrading viral RNA and limited cytotoxicity toward parasites, with C-mannosylation at key residues influencing its activity.^[39]^[41] Eosinophil peroxidase (EPO), a heme-containing enzyme with a molecular weight of about 66 kDa (comprising a 55 kDa heavy chain and 12.5 kDa light chain), catalyzes the oxidation of halides using hydrogen peroxide to produce hypohalous acids, such as hypobromous acid (HOBr) and hypochlorous acid (HOCl). This oxidative burst generates reactive species for pathogen destruction, including bromination of tyrosine residues in proteins and damage to helminth and bacterial targets; EPO's cationic nature (related to myeloperoxidase) localizes it to the granule matrix.^[39]^[42] Charcot-Leyden crystal protein (CLC/Gal-10), a 17 kDa galectin family member with pI ≈ 5.1–5.7, is stored in the eosinophil cytoplasm and forms characteristic hexagonal crystals upon cell activation or lysis in tissues. Its slightly acidic, hydrophobic properties promote self-assembly into crystals, serving as a hallmark of eosinophil involvement in diseases. As galectin-10, CLC modulates immune responses, including suppression of T-cell proliferation and acting as a carrier for eosinophil ribonucleases; it also serves as a biomarker for eosinophilic inflammation in conditions like asthma and eosinophilic esophagitis.^[39]^[43]^[44]^[45]

Degranulation Pathways

Eosinophils release their granule contents through distinct degranulation pathways that enable targeted immune responses, including compound exocytosis, piecemeal degranulation, and cytolysis. These mechanisms allow for both rapid bulk release and gradual, selective secretion of proteins such as major basic protein (MBP) and eosinophil cationic protein (ECP), depending on the inflammatory context.^[46] Compound exocytosis involves the fusion of multiple intracellular granules, which coalesce before simultaneously fusing with the plasma membrane to expel contents extracellularly. This pathway is triggered by calcium (Ca²⁺) influx, often initiated by immunoglobulin E (IgE) cross-linking on the eosinophil surface or complement component C5a activation, leading to rapid mediator release during acute responses.^[47]^[48] In contrast, piecemeal degranulation represents a more controlled process where granule contents are selectively transported via small vesiculotubular carriers, such as eosinophil sombrero vesicles, from maturing granules to the plasma membrane without full granule extrusion. This mechanism predominates in chronic inflammation, facilitating sustained release of mediators in tissues like those affected by allergic rhinitis or asthma, and is activated by chemokines including eotaxin and RANTES.^[49]^[50] Cytolysis occurs through non-apoptotic cell rupture, releasing intact granules and forming eosinophil extracellular traps (EETs) composed of mitochondrial DNA scaffolds decorated with granule proteins like MBP and ECP. This pathway is induced by stimuli such as lipopolysaccharide (LPS) from bacteria, contributing to antimicrobial defense in severe inflammatory settings, though its regulation remains incompletely understood.^[51]^[46] Degranulation is tightly regulated to prevent excessive tissue damage; for instance, engagement of the inhibitory receptor Siglec-8 on eosinophils suppresses these pathways by promoting apoptosis and reducing mediator release via Src family kinase signaling. Conversely, priming with interferon-gamma (IFN-γ) enhances eosinophil responsiveness, promoting piecemeal degranulation through mobilization of vesicular transport proteins like VAMP-2, without necessarily increasing cationic protein secretion.^[52]^[48]

Clinical Significance

Normal Counts and Assessment

The absolute eosinophil count (AEC) in peripheral blood, which quantifies the number of eosinophils per microliter, typically ranges from 0 to 500 cells/μL in healthy adults, though some laboratories establish an upper limit of less than 350 cells/μL.^[53]^[54] Eosinophils normally constitute 1% to 6% of total leukocytes in adults, reflecting their minor role in steady-state circulation.^[55] In children, reference ranges vary by age; neonates often exhibit higher counts, with a mean AEC around 550 cells/μL (ranging up to 1,300 cells/μL), which gradually decline toward adult levels by infancy.^[56]^[57] Eosinophil levels in blood are primarily assessed through a complete blood count (CBC) with differential, performed using automated hematology analyzers that employ flow cytometry or impedance-based methods to enumerate cell types based on size and granularity, or via manual microscopy of a Wright-Giemsa-stained blood smear for confirmation.^[53]^[58] Bone marrow biopsies, stained with hematoxylin and eosin or examined via aspirate smears, provide insight into eosinophil precursors (eosinophil promyelocytes and myelocytes) and maturation stages, particularly when peripheral counts are inconclusive.^[58] Tissue eosinophil assessment requires biopsy sampling followed by histopathological evaluation; immunohistochemistry using antibodies like anti-EG2, which targets activated eosinophils via eosinophil cationic protein (ECP), enables specific identification and quantification in inflamed tissues such as skin or mucosa.^[59] Alternatively, flow cytometry on enzymatically dissociated tissue samples can detect eosinophils by surface markers (e.g., CD45, Siglec-8) and intracellular granule proteins, offering quantitative analysis of cell populations in contexts like lung or gastrointestinal biopsies.^[60]^[61] Normal eosinophil counts can fluctuate due to physiological factors, including age-related elevations in neonates, a circadian rhythm with peak levels occurring at night (up to 20-30% diurnal variation), and ethnic differences, such as higher baseline counts observed in certain African and Asian populations compared to Caucasians.^[62]^[63] Counts exceeding these reference ranges may indicate pathological eosinophilia, as explored further in the section on Eosinophilia and Hypereosinophilia.^[64]

Eosinophilia and Hypereosinophilia

Eosinophilia is defined as an absolute eosinophil count exceeding 500 cells per microliter (μL) in peripheral blood.^[3] It is classified by severity into mild (500–1,500 cells/μL), moderate (1,500–5,000 cells/μL), and severe (>5,000 cells/μL), reflecting the degree of elevation and potential clinical implications.^[3] Hypereosinophilia refers to a more pronounced elevation, typically an absolute eosinophil count greater than 1,500 cells/μL on at least two occasions separated by one month or more.^[65] Hypereosinophilic syndrome (HES) is diagnosed when hypereosinophilia persists and is accompanied by evidence of organ dysfunction attributable to eosinophil infiltration, after exclusion of other potential causes of the damage.^[65] Diagnostic criteria for HES include a persistently elevated absolute eosinophil count >1.5 × 10⁹/L and evidence of organ damage attributable to eosinophilia, after excluding secondary causes. Bone marrow examination may show eosinophilia (>20% in clonal variants) to assess for underlying neoplasms.^[66] Elevations in eosinophil counts are etiologically classified into primary (clonal), secondary (reactive), and idiopathic forms. Primary eosinophilia arises from clonal proliferation of eosinophils due to underlying myeloid or lymphoid neoplasms, such as those involving PDGFRA rearrangements (e.g., FIP1L1-PDGFRA fusion), chronic myeloid leukemia, or myelodysplastic syndromes.^[67] Secondary eosinophilia is a reactive response to external triggers, commonly including allergic conditions, parasitic infections (particularly helminths), and drug reactions, driven by cytokine-mediated mechanisms.^[67] Idiopathic HES is a diagnosis of exclusion, occurring when no clonal or reactive cause is identified despite persistent hypereosinophilia with organ involvement.^[67] The pathophysiology of eosinophilia and hypereosinophilia involves dysregulated eosinophil production, maturation, and survival, often centered on interleukin-5 (IL-5) signaling. In reactive forms, excessive IL-5 production—typically from T cells or other immune cells—promotes eosinophilopoiesis in the bone marrow and inhibits apoptosis, leading to prolonged circulation and tissue accumulation.^[68] In clonal variants, genetic abnormalities such as fusion tyrosine kinase mutations (e.g., FIP1L1-PDGFRA) confer autonomous growth to eosinophil precursors, independent of external cytokines, resulting in unchecked proliferation and enhanced survival.^[68] Prognosis varies markedly by etiology. Reactive eosinophilia generally resolves upon identification and elimination of the underlying trigger, such as antiparasitic treatment for infections, leading to normalization of counts and alleviation of symptoms.^[69] In contrast, clonal forms like PDGFRA-rearranged HES carry a more guarded outlook without intervention, often progressing to organ damage, but respond well to targeted therapies such as tyrosine kinase inhibitors, achieving rapid remission in responsive cases.^[69]

Associated Diseases and Conditions

Eosinophils play a central role in the pathogenesis of various allergic disorders, where they contribute to type 2 inflammation through cytokine-driven recruitment and degranulation, leading to tissue damage in affected organs.^[70] In asthma, airway eosinophilia promotes bronchial remodeling by releasing granule proteins and mediators that induce mucus hypersecretion, smooth muscle hypertrophy, and subepithelial fibrosis, exacerbating airflow obstruction.^[71] Atopic dermatitis involves skin infiltration of eosinophils, which amplify chronic inflammation via release of cytotoxic proteins like major basic protein, contributing to epidermal barrier dysfunction and pruritus.^[72] Similarly, in allergic rhinitis, eosinophils accumulate in nasal mucosa, driving symptoms such as congestion and sneezing through degranulation and cytokine production that perpetuate Th2 responses.^[70] Gastrointestinal disorders associated with eosinophils include eosinophilic esophagitis (EoE) and eosinophilic gastroenteritis, characterized by selective eosinophil-rich inflammation in the digestive tract.^[73] In EoE, esophageal infiltration by eosinophils, often exceeding 15 per high-power field, leads to dysphagia and food impaction due to progressive fibrosis and stricture formation, triggered by food allergens in a Th2-mediated process.^[73] Eosinophilic gastroenteritis features eosinophil accumulation in the stomach, small intestine, or colon, causing abdominal pain, nausea, and malabsorption through mucosal and transmural inflammation, with mechanisms involving dysregulated IL-5 signaling.^[71] Hematologic conditions linked to eosinophils encompass hypereosinophilic syndrome (HES) and drug-induced eosinophilia, where persistent eosinophilia results in multi-organ damage.^[74] HES, defined by persistently elevated blood eosinophil counts above 1.5 × 10⁹/L (confirmed on at least two occasions at least one month apart) with evidence of organ involvement attributable to eosinophilia, often manifests as cardiac endomyocardial fibrosis leading to restrictive cardiomyopathy, pulmonary infiltrates causing respiratory distress, and neurologic deficits from thrombosis or infiltration.^[65] Drug-induced eosinophilia arises from hypersensitivity reactions to medications, resulting in acute tissue eosinophilia that can affect the skin, lungs, or liver, mediated by immune activation and cytokine release.^[70] In parasitic and infectious contexts, eosinophils are key effectors against helminth invasions, particularly tissue-migrating larvae, though they are less prominent in bacterial or viral infections except in specific vasculitides.^[71] During strongyloidiasis, eosinophils eliminate migrating Strongyloides stercoralis larvae in skin and intestinal tissues via antibody-dependent cytotoxicity and extracellular trap formation, limiting dissemination and contributing to protective immunity.^[75] Eosinophilic granulomatosis with polyangiitis (EGPA, formerly Churg-Strauss syndrome) features eosinophil-driven vasculitis affecting lungs, skin, and nerves, with mechanisms involving, in ANCA-positive cases (about 30-40%), endothelial damage associated with ANCA, alongside IL-5 overexpression in type 2 inflammation.^[76]^[70] Beyond these, eosinophils exhibit dual roles in tumors and fibrosis, influencing disease progression through cytotoxic and profibrotic activities. In various cancers, including oral tumors, eosinophils infiltrate the tumor microenvironment and exert anti-tumor effects via granule proteins such as eosinophil cationic protein and eosinophil peroxidase, which directly induce tumor cell apoptosis, though they can also promote angiogenesis in some contexts.^[77] In fibrotic processes, eosinophils contribute to tissue remodeling by releasing transforming growth factor-β (TGF-β), driving collagen deposition and extracellular matrix accumulation in organs like the heart and lungs during chronic inflammation.^[71]

Diagnosis and Management

Diagnosis of eosinophil-related disorders, such as hypereosinophilia and hypereosinophilic syndrome (HES), requires a systematic workup to identify underlying causes and assess organ involvement. A detailed patient history is essential, focusing on exposures to allergens, travel history suggesting parasitic infections, medications, and symptoms of end-organ damage like cardiac or pulmonary issues.^[65] Stool examinations for ova and parasites, along with serologic tests for infections, are performed to rule out reactive eosinophilia from helminthic causes.^[78] Imaging studies, including echocardiography to evaluate cardiac involvement in HES and chest CT for pulmonary infiltrates, help detect organ damage.^[79] Bone marrow aspiration and biopsy are indicated in persistent cases to quantify eosinophil infiltration (typically >20% of nucleated cells) and exclude clonal disorders.^[65] Genetic testing, particularly for the FIP1L1-PDGFRA fusion via fluorescence in situ hybridization (FISH) or reverse transcription polymerase chain reaction (RT-PCR), is crucial for identifying myeloid neoplasms associated with eosinophilia.^[80] Biomarkers play a supportive role in confirming eosinophil activation and differentiating from overlapping conditions. Serum levels of eosinophil cationic protein (ECP) and eosinophil-derived neurotoxin (EDN) are elevated in active disease and correlate with tissue damage, aiding in monitoring response to therapy.^[65] Tryptase levels may be assessed to evaluate for mast cell involvement in variant HES.^[79] Management prioritizes addressing the underlying cause when identifiable, followed by targeted suppression of eosinophil production and activity to prevent organ damage. For reactive eosinophilia due to parasites, antiparasitic agents such as ivermectin (200 mcg/kg/day for 2 days) are used, while allergen avoidance is recommended for atopic triggers.^[65] Corticosteroids remain first-line therapy for idiopathic or corticosteroid-responsive HES, with prednisone initiated at 1 mg/kg/day orally or high-dose intravenous methylprednisolone (1 g/day) for severe presentations, tapered based on clinical response and eosinophil counts.^[65] In cases with FIP1L1-PDGFRA fusion, tyrosine kinase inhibitors like imatinib (100 mg daily) provide targeted remission.^[80] Biologic therapies targeting interleukin-5 (IL-5) are increasingly used for steroid-dependent or refractory HES and severe eosinophilic asthma. Mepolizumab, an anti-IL-5 monoclonal antibody, is administered subcutaneously at 300 mg (as three 100 mg injections) every 4 weeks to reduce eosinophil counts and exacerbations.^[81] For severe eosinophilic asthma, reslizumab (3 mg/kg intravenously every 4 weeks) or benralizumab (30 mg subcutaneously every 4 weeks initially, then every 8 weeks) offer additional IL-5 pathway inhibition. Emerging data from phase 3 trials (as of November 2025) suggest benralizumab may benefit refractory HES.^[82]^[80] Ongoing monitoring is vital to assess treatment efficacy and complications. Serial absolute eosinophil counts (AEC), along with organ function tests (e.g., liver and renal panels, electrocardiograms, pulmonary function), guide therapy adjustments.^[79] Long-term corticosteroid use necessitates surveillance for side effects, including osteoporosis, diabetes, and infections, often requiring maintenance doses as low as 10 mg/day prednisone.^[65] Multidisciplinary follow-up, including cardiology and pulmonology consultations, ensures comprehensive care for associated organ involvement.^[78]

Research Perspectives

Insights from Animal Models

Animal models, particularly murine systems, have been instrumental in elucidating the mechanistic roles of eosinophils in development, host defense, and inflammatory pathologies. In IL-5 transgenic mice engineered for lung-specific IL-5 overexpression, constitutive cytokine production drives marked pulmonary eosinophilia, accompanied by airway hyperreactivity to methacholine, goblet cell hyperplasia, epithelial hypertrophy, and focal collagen deposition—features pathognomonic of asthma—without requiring allergen challenge.^[83] Similarly, GATA1 knockout mice reveal profound developmental defects in the eosinophil lineage, with a complete absence of IL-5-responsive eosinophil progenitors in fetal liver and no mature eosinophils detectable in peripheral tissues, establishing GATA1 as an essential transcription factor for eosinophil commitment and maturation.^[84] Parasitic infection models further highlight eosinophils' effector functions in helminth immunity. During Schistosoma mansoni infection in mice, eosinophils mediate antibody-dependent cellular cytotoxicity (ADCC) against schistosomula, with lung lavage cells from immunized animals achieving up to 51% greater parasite killing in the presence of immune sera, involving nitric oxide production and collaboration with macrophages as key effectors.^[85] Eosinophils also deploy extracellular traps (EETs) at infected sites, releasing DNA webs laden with granule proteins to ensnare and damage parasites, thereby contributing to granuloma formation and worm clearance.^[86] In eotaxin-deficient mice challenged with nematodes like Nippostrongylus brasiliensis, eosinophil recruitment to skin and other tissues is significantly impaired—evidenced by reduced infiltration following larval injection—demonstrating eotaxin's critical role in chemotactic guidance during primary infections, though it proves less essential for gut expulsion.^[87] Allergic sensitization models underscore eosinophils' contributions to Th2 polarization and tissue remodeling. In ovalbumin (OVA)-sensitized and challenged mice, eosinophils are required for robust Th2 responses, as eosinophil-deficient strains exhibit diminished IL-4, IL-5, and IL-13 production alongside reduced effector T cell recruitment to the lungs; adoptive transfer of eosinophils restores chemokine expression (e.g., TARC/CCL17 and MDC/CCL22) and full Th2-driven inflammation.^[88] Eosinophils promote fibrosis in these contexts, with their derived leukotriene C4 (LTC4) signaling through the type 2 cysteinyl leukotriene receptor (CysLT2R) to enhance collagen synthesis in fibroblasts and epidermal proliferation, as LTC4 synthase-deficient or CysLT2R-knockout mice show markedly attenuated dermal thickening and collagen deposition post-OVA exposure.^[89] The ΔdblGATA mouse, which selectively ablates eosinophils via targeted GATA1 mutation without affecting other lineages, serves as a foundational tool for modeling hypereosinophilia by contrasting eosinophil-dependent pathologies, such as exacerbated allergic responses or impaired parasite control in reconstitution experiments.^[90] Despite these insights, murine models carry inherent limitations that temper their translational value. A notable species difference is the absence of Siglec-8 on mouse eosinophils, a human inhibitory receptor that triggers apoptosis upon ligation; mice instead express Siglec-F, which shares sialic acid-binding specificity but lacks expression on mast cells and exhibits inflammation-dependent upregulation, complicating direct parallels in regulatory mechanisms.^[91] Moreover, these models predominantly emphasize eosinophils' pathological contributions in allergy and infection, often overlooking their homeostatic roles in tissue repair and immune surveillance observed in steady-state conditions.

Emerging Human Studies and Therapies

Recent human studies have identified distinct eosinophil subtypes, including resident eosinophils (rEos) and inflammatory eosinophils (iEos), with transcriptomic differences aligning with functional roles in homeostasis versus pathology, such as in severe asthma and chronic rhinosinusitis.^[46]^[92] These subtypes exhibit differential functions, with resident forms supporting regulatory roles in steady-state tissues and inflammatory variants driving type-2 immune responses in diseases like eosinophilic esophagitis (EoE) and hypereosinophilic syndrome (HES).^[92] Single-cell RNA sequencing of circulating eosinophils from asthma patients has further revealed transcriptomic heterogeneity, highlighting CD62L-based clustering that aligns with these functional distinctions.^[93] The NATRON Phase III trial, completed in 2025, demonstrated that benralizumab, an anti-IL-5 receptor monoclonal antibody, significantly delayed the time to first disease flare or worsening in patients with HES when added to standard therapy, reducing the risk by over 50% compared to placebo over 24 weeks.^[82] Similarly, the DEGAS Phase II trial, with results presented in 2025, showed that dupilumab, targeting IL-4 and IL-13 signaling, reduced peak gastric eosinophil counts by more than 90% in patients with eosinophilic gastritis, a condition overlapping with EoE pathology, alongside improvements in symptoms and endoscopic features. Emerging evidence also points to gut microbiome influences on eosinophil activation, with 2024 studies indicating that microbial dysbiosis can enhance type-2 inflammation via IL-5 production, potentially exacerbating allergic conditions.^[94] Novel insights from 2024 research underscore eosinophils' roles in colitis, where they respond to bacterial pathogens like Salmonella by accumulating in gut-draining lymph nodes, though they are not essential for pathogen clearance.^[95] In EoE, targeting the transcription factor FOXM1 has shown promise for restoring epithelial repair, as FOXM1 inhibition in patient-derived models reduced basal cell proliferation and improved barrier integrity, alleviating remodeling associated with eosinophil-driven damage.^[96] Expanded use of anti-IL-4/IL-13 biologics, such as dupilumab, is advancing for broader eosinophilic diseases, with 2025 studies confirming histologic remission rates of 60-84% in EoE and related gastrointestinal disorders at 16-52 weeks, alongside reduced exacerbations in severe asthma.^[97] Future directions in eosinophil research emphasize gene editing strategies for clonal HES, where CRISPR-based approaches to hematopoietic stem cells are being explored to correct driver mutations like those in PDGFRA, building on preclinical models of clonal hematopoiesis to prevent eosinophil expansion. Personalized medicine is also gaining traction through eosinophil transcriptomics, with single-cell analyses in 2024-2025 identifying eosinophil heterogeneity that may predict treatment responses in EoE and asthma, enabling tailored biologics based on subtype-specific gene expression profiles.^[98] These advances, supported by omics integration, hold potential for precision therapies targeting eosinophil heterogeneity across inflammatory conditions.^[99]

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