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An Official Publication of the Indian Association of Oral and Maxillofacial Pathologists


 
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Year : 2003  |  Volume : 7  |  Issue : 2  |  Page : 31-33
 

Eosinophils in health and disease: An overview


Department of Oral Pathology. Ragas Dental College and Hospital, Chennai, India

Correspondence Address:
S Nalinkumar
Department of OP, Ragas Dental College and Hospital 21102, East coast road Uthandi, Chennai 119
India
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Source of Support: None, Conflict of Interest: None


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   Abstract 

Eosinophils are granulocytes, which are present in a variety of diseases. They perform numerous important functions and play a key role in defense against various diseases. The structure, contents of granules, functions, activation, emigration, infiltration and degranulation of eosinophils are discussed in this article. Eosinophilia and associated oral diseases are also mentioned.


Keywords: Eosinophils, parasitic infections, hypersensitivity, granules, eotaxin.


How to cite this article:
Saraswathi T R, Nalinkumar S, Ranganathan K, Umadevi R, Elizabeth J. Eosinophils in health and disease: An overview. J Oral Maxillofac Pathol 2003;7:31-3

How to cite this URL:
Saraswathi T R, Nalinkumar S, Ranganathan K, Umadevi R, Elizabeth J. Eosinophils in health and disease: An overview. J Oral Maxillofac Pathol [serial online] 2003 [cited 2019 Aug 22];7:31-3. Available from: http://www.jomfp.in/text.asp?2003/7/2/31/40933



   Introduction Top


Eosinophils are bone marrow derived granulocytes and are found in abundance in hypersensitivity reactions and parasitic infections [1] . They were discovered by Paul Ehrlich in 1879. They can be distinguished from othergranulocytes by the affinity of their cytoplasmic granules for acidic stains like eosin; resulting in intense red staining, which gives them their name [2] .

Lineage ofeosinophils

Hematopoiesis or generation of blood cells occurs in the bone marrow in adults. All the blood cells originate from a common stem cell, which becomes committed to differentiate along particular lineages. This pluripotent stem cell broadly differentiates into a myeloid progenitor cell or a lymphoid progenitor cell. The lymphoid progenitor cell gives rise to the lymphocytes, whereas the myeloid progenitor cell differentiates along different lineages namely erythroid, megakaryocytic, granulocytic and monocytic. The myeloid progenitor cell differentiates along one particular lineage called eosinophil colony forming unit (CFIJ-Eo) and forms eosinophils [2] . Bone marrow generation of eosinophils is regulated by interleukin-5 and the release from the circulation into the tissues requires the action of several chcmokines, cytokines and adhesion molecules [13]

Structure of eosinophils

Eosinophils comprise about 1-3% of white blood cells in the blood. The normal range of eosinophils is 40-450 cells/cu. mm. The diameter of an cosinophil is 10-12 microns. The eosinophil is characterized by its abundant cytoplasm with coarse reflective granules, which stain red [2] . These granules appear as rod like crystalloid inclusions when viewed by electron microscope. The nucleus is in the shape of two lobes connected by a bridge.

Contents of eosinophil granules

The eosinophil has many proinflammatory mediators with considerable potential to initiate and sustain an inflammatory response. These include cylotoxic granule proteins, cytokines, chemokines, and lipid mediators [3] . The proteins present in the eosinophil granules include Major Basic Protein (MBP), Eosinophil Cationic Protein (ECP), Eosinophil Derived Neurotoxin (EDN), Eosinophil Peroxidase (EPO), aryl sulfatase and hydrolytic enzymes [3],[4],[5] .

Functions of eosinophils

Eosinophils play a protective role in host immunity to infections by parasitic worms and are involved in the pathophysiology of asthma and other allergic diseases [3],[5] . The cytoplasmic granules are toxic to parasitic worms and limit the extent of worm infestations [6] . Eosinophils mediate a special type of Antibody Directed Complement Cytotoxicily (ADCC) against some helminthic parasites [5] , Eosinophils also contain histaminase that may modulate mast cell mediated inflammation [7] and collagenase, which may aid in remodelling connective tissue during healing. Eosinophils are also involved in the killing of bacteria through eosinophilic peroxidase activity (3). Synthesis and expression of class II proteins of the major histocompatibility complex (MIIC) may enable eosinophils to serve as antigen-presenting cells [6]


   Eosinophil Activation Top


Eosinophil activation involves chemotactic factors for eosinophils, namely worm extracts, histamine and eosinophilic chemotactic factor A in mast cells. neutrophil peptides, eosinophil stimulator & promoter substances in lymphocytes, C5a complement and eotaxin. Eotaxin is a novel eosinophil-selective chemoattractant, that plays a major role in eosinophil recruitment in allergic inflammation and parasitic diseases [8] .

There are many methods of eosinophil activation. Eosinophils are activated by phosphorylation of signal transducing proteins within the eosinophils, which will lead to release of granules by exocytosis. Activated eosinophils produce Platelet Activating Factor (PAF), which acts as an autocrine substance to increase the activated state of eosinophils. PAF is also produced by endothelial cells that will result in further activation of eosinophils. In addition, eosinophils also have receptors for IgA that can he activated as a result of cross-linking by antigens. Chemokines such as Regulated and Normal T-lymphocyte Expressed and Secreted (RANTES), cotaxin and Major Inflammatory Protein (MIP-1) are considered to be involved in the pathophysiology of allergic inflammation because of their ability to drive eosinophils through their binding sites, expressed on eosinophils [9] .

Eosinophil emigration

The recruitment of eosinophils to sites of allergic inflammation is a complex process that is mediated by inflammatory cytokines and chcmokines [10] . These molecules act to stimulate peripheral eosinophilia, and regulate homing of eosinophils to the inflamed site. They also promote eosinophil-vascular endotheliurn interactions, extravasation, chemotaxis, and localization to the site of the inflammatory stimulus [11]. Lymphocytes release cytokines, which recruit and activate eosinophils. These cytokines also generate adhesion molecules on endothelial cell surfaces that promote diapedesis of the eosinophils out of the circulation into the tissues. In the tissues, the eosinophils degranulate, releasing toxic proteins and thus perform their functions [12],[13] .

Eosinophil degranulation

Helminthes are too large to be engulfed by phagocytes. IgE coats these helminthes. Once eosinophils have emigrated into the tissues, they bind with this IgE. This is followed by degranulation of the eosinophils leading to the release of the toxic granules. MBP and I. CP present in the granules are responsible for the killing of the parasites [14] .

Degranulation of eosinophils in target tissues is considered a key pathogenic event in major chronic eosinophilic diseases [15] . Biopsy specimens tram patients with inflammatory bowel disease, allergic rhinitis, asthma, and nasal polyposis when evaluated with transmission electron microscopy display a similar degree of local tissue eosinophilia. In contrast, marked differences in the mean extent of eosinophil degranulation were observed between the patient groups. Different eosinophilic conditions, despite having similar number of tissue eosinophils, may exhibit markedly different degranulation patterns [16] .

Eosinophilia

Eosinophilia is defined as an increase in the number of eosinophils above 450/cu.mm It is not the actual disease process but the response to a disease. Eosinophilia is seen in allergic disorders like asthma, eczema, urticaria, angioneurotic edema, and drug sensitivity [17] . It is commonly present in parasitic infestations and skin disorders like pemphigus, bullous pemphigoid, erythema multiforme, Kimura's disease and angiolymphoid hyperplasia [18],[19] . Diseases of haematopoietic system like chronic myeloid leukemia, polycythemia vera, pernicious anaemia, myelofibrosis, and Hodgkin's lymphoma [20] also may exhibit eosinophilia. Eosinophilia is present in collagen vascular diseases like rheumatoid arthritis, periarteritis and systemic lupus erythematosus [19] . Eosinophilia can be present in malignant disease of any type especially with metastasis. Miscellaneous causes of eosinophilia include X-ray irradiation, sarcoidosis, eosinophiliamyalgia syndrome and hypereosinophilia syndrome [19] .

Eosinophils and oral diseases

In the head and neck region, eosinophilia is present in many diseases Eosinophilia is seen in reactive lesions of the oral cavity like allergic gingivitis and lichenoid mucositis. Lichenoid mucositis are lesions that are clinically identical to lichen planes occurring bilaterally or unilaterally. Histopathologically, it differs from lichen planes in that, the subepithelial lymphocytic infiltrate lacks the well-defined "band like appearance," being more diffuse and deep. containing eosinophils and plasma cells. Perivascular infiltration is also seen in sonic cases [21] . Eosinophilia is present in vesiculobullous lesions like pemphigus, erythema multiforme, and the like [24] . Patients affected with oral fungal lesions present with eosinophilia [25] . Eosinophilia is frequently seen in patients suffering from parasitic infections like cysticercosis [22] , hydatid cyst and filariasis [23] . A rare oral lesion associated with eosinophilia is Traumatic Ulcerated Granuloma with Stromal Eosinophilia (TUGSE) [26],[27] . Kimura's disease [28] and Langerhans cell histiocytosis [29] are other diseases that stay manifest in the oral cavity having an association with eosinophils.


   Conclusion Top


Eosinophils are granulocytes, which are present in a variety of diseases. They are multi faceted cells, which perform an array of functions. Eosinophilia is seen in wide spectrum of diseases ranging from simple allergy to malignancy with metastasis. In patients with eosinophilia, it is prudent to have a thorough investigation performed to diagnose and rule out any underlying systemic disease.

 
   References Top

1.Gleich GJ, Ottesen EA, Leiferman KM et al (1989): Eosinophils and human disease, Int Arch Allergy Appl Immunol, 88(1-2): 59-62.  Back to cited text no. 1    
2.Roitt I, Brostoff J, Male D: Immunology, (5 th ed.), Mosby publications, pages: 29-30 & 156.  Back to cited text no. 2    
3.Chihara J (1996): The role of adhesion molecules, cytokines, and chemokines in cosinophil activation during allergic inflammation, Nihon Kyobu Shikkan Gakkai Lasshi, 34, Suppl: 116-20.  Back to cited text no. 3    
4.Walsh GM (2001): Eosinophil granule proteins and their role in disease, Cure Opin Hematol, 8(1): 28-33.  Back to cited text no. 4    
5.Bruijnzeel PL, Rihs S, Betz S (1992): Eosinophilic granulocytes and their significance in allergic diseases, Schweiz Mod Wochenschr, 8, 122(6): 173-80.  Back to cited text no. 5    
6.Walsh GM (1999): Advances in the immunobiology of eosinophils and their role in disease, Crit Rev Clin Lab Sci, 36(5): 453-96.  Back to cited text no. 6    
7.KroegeI C, Luttmann W, Zeck-Kapp G et al (1994): Cell biology and function of eosinophilic granulocytes in immunologic inflammation. Immun Infekt, 22(3): 104-13.  Back to cited text no. 7    
8.Bandeira-Melo C, Cordeiro RS, Silva PM et al (1997): Modulatory role of eosinophils in allergic inflammation: new evidence for a rather outdated concept, Mem Inst Oswaldo Cruz. 92, Suppl, 2:37-43.  Back to cited text no. 8    
9.Chihara J (1998): The role of chemokines such as RANTES in allergic disease, Rinsho Byori, 46(8): 816-20.  Back to cited text no. 9    
10.Rankin SM, Conroy DM, Williams TJ (2000): Eotaxin and eosinophil recruitment: implications for human disease, Mol Med Today, 6(1): 20-7.  Back to cited text no. 10    
11.Hogan SP, Foster PS (1996): Cellular and molecular mechanisms involved in the regulation of eosinophil trafficking in vivo, Med Res Rev, 16(5):407-32.  Back to cited text no. 11    
12.Broide D, Sriramarao P (2001): Fosinophil trafficking to sites of allergic inflammation: Immunol Rev, 179:163-72.  Back to cited text no. 12    
13.Reed CF. (1994): The importance of eosinophils in the immunology of asthma and allergic disease, Ann Allergy, 72(4): 376-80.  Back to cited text no. 13    
14.Martin LB, Kita H, Leiferman KM (1996): Eosinophils in allergy: role in disease, degranulation, and cytokincs, Int Arch Allergy Immunol, 109(3): 207-15.  Back to cited text no. 14    
15.Kato M, Kephart GM, Talley NJ, et al (1998): Eosinophil infiltration and degranulation in normal human tissue, Anat Rec, 252(3): 418-25.  Back to cited text no. 15    
16.Erjefalt JS, Greiff L, Andersson M et at (2001): Degranulation patterns of eosinophil granulocytes as determinants of eosinophil driven disease, Thorax, 56(5): 341-4.  Back to cited text no. 16    
17.Kay AB (1985): Eosinophils: role in asthma, allergy and parasite immunity, N Engl Reg Allergy Proc, 6(4): 341-5.  Back to cited text no. 17    
18.Leiferman KM (1991): A current perspective on the role of eosinophils in dermatologic diseases, J Am Acad Dermatol, 24(6 Pt 2): 1101-12.  Back to cited text no. 18    
19.Gleich GJ, Adolphson CR (1986): The eosinophilic leukocyte: structure and function, Adv Immunol, 39:177-253.  Back to cited text no. 19    
20.Butterfield JH, Kephart GM, Gleich GJ (1986): Extracellular deposition of eosinophil granule major basic protein in lymph nodes of patients with Hodgkin's disease, Blood, 68(6): 1250-6.  Back to cited text no. 20    
21.McCartan BE, Lamey PJ (1997): Expression of CD1 and HI.A-DR by langerhans cells (LC) in oral lichenoid drug eruptions (LDE) and idiopathic oral lichen plan us (LP), J Oral Pathol Med, 26:176-80.  Back to cited text no. 21    
22.Fabbri P, Caproni M, Berti S et al (2003): The role of T lymphocytes and cytokines in the pathogenesis of pemphigoid gestations, Br J Dermatol, 148(6): 114-18.  Back to cited text no. 22    
23.Wagner JM, Franco M, Kephart GM et al (1998): Localization of eosinophil granule major basic protein in paracoccidioidomycosis lesions, Am J Trop Med I lyg, 59(1): 66-72.  Back to cited text no. 23    
24.Elizabeth J, Saraswathi TR, Ranganathan K (2003): Oral Cysticercosis, Journal of Indian Association of Oral Medicine and Radiology, 5(1): 10-12.  Back to cited text no. 24    
25.Rajendran R, Sunish IP, Mani TR et al (2002): Targeting of children in filariasis mass drug administration, Lancet, 360(9343): 1430.  Back to cited text no. 25    
26.Mezei MM, Tron VA, Stewart WD et al (1995): Eosinophilic ulcer of the oral mucosa, J Am Acad Dermatol, 33:734-40.  Back to cited text no. 26    
27.El-Mofty SK, Swanson PE., Wick M R ct al (1993): Eosinophilic ulcer of the oral mucosa. Report of 38 new cases with IHC observations, Oral Surg Oral Mod Oral Pathol, 75(6): 716-22.  Back to cited text no. 27    
28.Ray V, Boisscau-Garsaud AM, Billion G (2003): Kimura's disease on the hard palate in a patient from Martinique, Rev Med Interne, 24(4):253-6.  Back to cited text no. 28    
29.Milian MA, Bagan JV, Jimenez Y et al (2001): Langerhans cell histiocytosis restricted to oral mucosa, Oral Surg Oral Mod Oral Pathol, 91(1):76-9.  Back to cited text no. 29    




 

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    Abstract
    Introduction
    Eosinophil Activ...
    Conclusion
    References

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