The role of eosinophils in asthma
Faris Q. Alenzi, Fahad G. B. Alanazi, Abdulaziz D. Al-Faim, Mohamed W. Al-Rabea, Waleed Tamimi, Bassel Tarakji, Omar Kujan, Ali Al-Jabri, Richard K. H. Wyse
College of Applied Medical Sciences, Salman bin Abdulaziz University, Al-Kharj, Saudi Arabia.
College of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Department of Microbiol & Immunology, College of Medicine, Sultan Qaboos University, Muscat, Oman.
Department of Pathology and Laboratory Medicine, King Abdulaziz Medical City, Riyadh, Saudi Arabia.
Department of Pathology, Al-Farabi Medical College, Riyadh, Saudi Arabia.
Department of Pharmacy, Ministry of Health, Riyadh, Saudi Arabia.
Department of Preventive Medicine, Ministry of Health, Riyadh, Saudi Arabia.
Imperial College of Medicine, London, UK.
DOI: 10.4236/health.2013.52A045   PDF    HTML   XML   5,682 Downloads   9,103 Views   Citations

Abstract

Asthma is a chronic inflammatory disorder of the airways characterized by recurring episodes of reversible airway obstruction, hyper-responsiveness, wheezing, breathlessness and coughing. Clinical diagnosis of asthma is based on the pattern of clinical symptoms and pulmonary fuction tests. Asthma affectes 5% - 10% of the population and the number of worldwide cases is approximately 300 milliones. The incidence of this disease is increasing particulry in western countries [1]. It is the cause of a huge economic burden to national healthcare services. In a minority of cases, asthma is potentially fatal. After a period when fatalities appeared to be increasing [2], in recent years asthma-related mortality has progressively declined due to the develop- ment of specific asthma disease management programs, as well as the extensive use of in- haled corticosteroids [3]. Inflammation of the airways is a central component in asthma. In- flammation is associated with infliltration of the airway wall with eosinophiles and or neutron- philes mast cell degranulation and T cell active- tion. Other pathological features include, sub- basement membrane thickening, loss of epithet- lial cell integrity, goblet cells hyperplasia In- crease in airway smooth muscle mass. Eosino- phils are thought to be vital in the development of airway hyperreactivity, with the eosinophil cationic protein playing a crucial role [4]. The fact that treatment of asthma with corticos-teroids reduces eosinophils numbers and decreases airway reactivity further supports this hypothesis.

Share and Cite:

Alenzi, F. , Alanazi, F. , Al-Faim, A. , Al-Rabea, M. , Tamimi, W. , Tarakji, B. , Kujan, O. , Al-Jabri, A. and Wyse, R. (2013) The role of eosinophils in asthma. Health, 5, 339-343. doi: 10.4236/health.2013.52A045.

Conflicts of Interest

The authors declare no conflicts of interest.

References

[1] (2008) World Health Organisation. http://www.who.int/mediacentre/factsheets/fs307/en/print.html
[2] Sears, M.R., Barnes, P.J., Rodger, I.W. and Thomson, N.C. (1998) Epidemiology. Asthma: Basic mechanisms and clinical management. Academic Press, San Diego, 1-33.
[3] Rubin, B.K. and Pohanka, V. (2012) Beyond the guide- lines: Fatal and near-fatal asthma. Paediatric Respiratory Reviews, 13, 106-111. doi:10.1016/j.prrv.2011.05.003
[4] Bystrom, J. and Amin, K. (2011) Bishop-bailey D. Ana- lysing the eosinophil cationic protein—A clue to the function of the eosinophil granulocyte. Respiratory Research, 12, 10. doi:10.1186/1465-9921-12-10
[5] Venge, P.E. (1998) Asthma: Basic mechanisms and clinical management. In: Barnes, P.J., Rodger, I.W. and Thomson, N.C., Eds., Academic Press, San Diego, 1-33.
[6] Gleich, G.J., Adolphson, C.R. and Leiferman, K.M. (1993) The biology of the eosinophilic leukocyte. Annual Review of Medicine, 44, 85-101. doi:10.1146/annurev.me.44.020193.000505
[7] Spry, C.J.F. (1998) Eosinophils: A comprehensive review and guide to the scientific and medical literature. Oxford University Press, Ox-ford, 1998.
[8] Denburg, J.A. (1998) The origins of basophils and eosinophils in allergic inflammation. Journal of Allergy and Clinical Immunology, 102, S74-S76. doi:10.1016/S0091-6749(98)70034-X
[9] Rosenberg, H.F., Phipps, S. and Foster, P.S. (2007) Eosinophil trafficking in allergy and asthma. Journal of Al- lergy and Clinical Immunology, 119, 1303-1310. doi:10.1016/j.jaci.2007.03.048
[10] Sanderson, C.J. and Urwin, D. (2000) Interleukin-5: A drug target for allergic diseases. Current Opinion in In- vestigational Drugs, 1, 435-441.
[11] Greenfeder, S., Umland, S.P., Cuss, F.M., Chapman, R.W. and Egan, RW. (2001) Th2 cytokines and asthma. The role of interleukin-5 in allergic eosinophilic disease. Respiratory Research, 2, 71-79. doi:10.1186/rr41
[12] Tanaka, H., Komai, M., Nagao, K., Ishizaki, M., Kajiwara, D., Takatsu, K., Delespesse, G. and Nagai, H. (2004) Role of interleukin-5 and eosinophils in allergen-induced airway remodeling in mice. American Journal of Respira- tory Cell and Molecular Biology, 31, 62-68. doi:10.1165/rcmb.2003-0305OC
[13] Leckie, M.J., tenBrinke, A., Khan, J., Diamant, Z., O’Connor, B.J., Walls, C.M., et al. (2000) Effect of inter-leukin-5 blocking monoclonal antibody on eosinophils, airway hyperresponsiveness and the late asthmatic re- sponse. Lancet, 356, 2144-2148. doi:10.1016/S0140-6736(00)03496-6
[14] O’Byrne, P.M., Inman, M.D. and Parameswaran, K. (2001) The trials and tri-bulations of IL-5, eosinophils, and allergic asthma. Journal of Allergy and Clinical Im- munology, 108, 503-508. doi:10.1067/mai.2001.119149
[15] Lipworth, B.J. (2001) Eo-sinophils and airway hyper- responsiveness. Lancet, 357, 1446. doi:10.1016/S0140-6736(00)04597-9
[16] Flood-Page, P.T., Menzies-Gow, A.N., Kay, A.B. and Robinson, D.S. (2003) Eosinophil’s role remains uncertain as anti-interleukin-5 only partially depletes numbers in asthmatic airway. American Journal of Respiratory and Critical Care Medicine, 167, 199-204. doi:10.1164/rccm.200208-789OC
[17] Huib, A.M.K., Michael, E., Ronald, D., Pierluigi, P., Ek- kehard, B., Mark, V., Ralf, S., Dipl, M., Wolfgang, S., Petra, M.-Z. and Eric, D.B. (2012) Tiotropium in asthma poorly controlled with standard combina-tion therapy. The New England Journal of Medicine, 367, 1198-1120
[18] Morokata, T., Ida, K. and Yamada, T. (2002) Characterization of YM-90709 as a novel antagonist which inhibits the binding of interleukin-5 to interleukin-5 receptor. In- ternational Immunopharmacology, 2, 1693-1702. doi:10.1016/S1567-5769(02)00191-1
[19] O’Byrne, P.M. (2011) Therapeutic strategies to reduce asthma exacerbations. Journal of Allergy and Clinical Immunology, 128, 257-263. doi:10.1016/j.jaci.2011.03.035
[20] Busse, W.W., Ring, J., Huss-Marp, J. and Kahn, J.E. (2010) A review of treatment with mepolizumab, an anti- IL-5 mAb, in hypereosinophilic syndromes and asthma. Journal of Allergy and Clinical Immu-nology, 125, 803- 813. doi:10.1016/j.jaci.2009.11.048
[21] Wenzel, S.E., Schwartz, L.B., Langmack, E.L., Halliday, J.L., Trudeau, J.B., Gibbs, R.L. and Chu, H.W. (1999) Evidence that severe asthma can be di-vided pathologically into two inflammatory subtypes with distinct physiologic and clinical characteristics. American Journal of Respiratory and Critical Care Medicine, 160, 1001-1008.
[22] Sexton, D.W., Blaylock, M.G. and Walsh, G. (2001) Human alveolar epithelial cells engulf apoptotic eosi-nophils by means of integrin- and phosphatidylserine receptor dependent mechanisms: A process upregulated by dexa- me-thasone. Journal of Allergy and Clinical Immunology, 108, 962-969.
[23] Schleimer, R.P. and Bochner, B.S. (1994) The effects of glucocorticoids on human eosinophils. Journal of Allergy and Clinical Immunology, 94, 1202-1213. doi:10.1016/0091-6749(94)90333-6
[24] Adachi, T., Motojima, S., Hirata, A., Fukuda, T., Kihara, N. and Kosaku, H. (1996) Eosinophil apoptosis caused by theophylline, glucocorticoids, and macrolides after stimulation with IL-5. Journal of Allergy and Clinical Immunology, 98, S207-S215. doi:10.1016/S0091-6749(96)70068-4
[25] Sexton, D.W., Al-Rabia, M.W., Blaylock, M.G. and Walsh, G.M. (2004) Pha-gocytosis of apoptotic eosinophils but not neutrophils by bron-chial epithelial cells. Clinical & Experimental Allergy, 34, 1514-1524. doi:10.1111/j.1365-2222.2004.02054.x
[26] Schleimer, R.P. (1990) Effects of glucocorticoids on inflammatory cells relevant to their therapeutic applications in asthma. American Review of Respiratory Disease, 141, S59-S69.
[27] Zhang, X., Moilanen, E. and Kankaanranta, H. (2000) Enhancement of human eosinophil apoptosis by fluticasone propionate, bude-sonide, and beclomethasone. European Journal of Pharmacology, 496, 325-332. doi:10.1016/S0014-2999(00)00690-7
[28] Meagher, L.C., Cousin, J.M., Seckl, J.R. and Haslett, C. (1996) Opposing effects of glucocorticoids on the rate of apoptosis in neutrophilic and eosinophilic granulocytes. The Journal of Immunology, 156, 4422-4428.
[29] Chauhan, S., Leach, C.H., Kunz, S., bloom, J.W. and Miesfeld, R.L. (2003) Glucocorticoid regulation of human eosinophil gene expression. Journal of Steroid Bio-chemistry and Molecular Biology, 84, 441-452. doi:10.1016/S0960-0760(03)00065-7
[30] Lilly, C.M., Naka-mura, H., Kesselman, H., Nagler- Anderson, C., Asano, K. and Garcia, Z.E.A. (1997) Expression of eotaxin by human lung epithelial cells-induction by cytokines and inhibition by glu-cocorticoids. Jour- nal of Clinical Investigation, 99, 1767-1773. doi:10.1172/JCI119341
[31] Ren, Y. and Savill, J. (1995) Proinflammatory cytokines potentiate thrombospondin-mediated phagocytosis of neutrophils undergoing apoptosis. The Journal of Immunology, 154, 2366-2374.
[32] Saunders, M.W., Wheatley, A.H., George, S.J., Lai, T. and Birchall, M.A. (1999) Do corticosteroids induce apoptosis in nasal polyp inflamma-tory cells? In Vivo and in Vitro studies. Laryngoscope, 109, 785-790. doi:10.1097/00005537-199905000-00019
[33] Woolley, K.L., Gibson, P.G., Carty, K., Wilson, A.J., Twaddell, S.H. and Wool-ley, M.J. (1996) Eosinophil apoptosis and the resolution of airway inflammation in asthma. American Journal of Respiratory and Critical Care Medicine, 154, 237-243.
[34] Liu, Y.Q., Cousin, J.M., Hughes, J., Van Damme, J., Seckl, J.R. and Has-lett, C. (1999) Glucocorticoids promote nonphlogistic phago-cytosis of apoptotic leukocytes. The Journal of Immunology, 162, 3639-3646.
[35] Duval, E., Wyllie, A.H. and Morris, R.G. (1985) Macro-phage recognition of cells undergoing programmed cell death (apoptosis). Immunology, 56, 351-358.
[36] Savill, J., Hogg, N., Ren, Y. and Haslett, C. (1992) Thrombospondin cooperates with CD36 and the vitronectin receptor in macrophage recognition of neutrophils undergoing apoptosis. Journal of Clinical Investigation, 90, 1513-1522. doi:10.1172/JCI116019
[37] Albert, M.L., Pearce, S.F.A., Francisco, L.M., Sauter, B., Roy, P. and Silverstein, R.L. (1998) Immature dendritic cells phagocytose apoptotic cells via αvβ5 and CD36 and cross present antigens to cytotoxic T lym-phocytes. The Journal of Experimental Medicine, 188, 1359-1368. doi:10.1084/jem.188.7.1359
[38] Finnemann, S.C., Bonilha, V.L., Marmorstein, A.D. and Rodriguez-Boulan, E. (1997) Phagocytosis of rod outer segments by retinal pigmented epithelial cells requires αvβ5 integrin for binding but not interna-lization. Proceedings of the National Academy of Sciences of the United States of America, 94, 12932. doi:10.1073/pnas.94.24.12932
[39] Fadok, V.A., Savill, J.S., Haslett, C., Bratton, D.L., Do- herty, D.E. and Campbell, PA. (1992) Different populations of macrophages use either the vitronectin receptor or the phosphatidylserine receptor to recognize and remove apoptotic cells. The Journal of Immunology, 149, 4029-4035.
[40] Fadok, V.A., Voelker, D.R., Campbell, P.A., Cohen, J.J., Bratton, D.L. and Henson, P.M. (1992) Exposure of phosphatidyl-serine on the surface of apoptotic lymphocytes triggers specific recognition and removal by macrophages. The Journal of Immunology, 148, 2207-2216.
[41] Platt, N., Suzuli, H., Kurihara, Y., Kodoma, T. and Gordon, S. (1996) Role for the class A scavenger receptor in the phagocytosis of apoptotic thymocytes in vitro. Proceedings of the National Academy of Sciences of the United States of America, 93, 12456-12460. doi:10.1073/pnas.93.22.12456
[42] Sambrano, G.R. and Steinberg, D. (1995) Recognition of oxidatively damaged and apoptotic cells by an oxidized low-density lipoprotein receptor on mouse peritoneal macrophages: Role of membrane phospha-tidylserine. Proceedings of the National Academy of Sciences of the United States of America, 92, 1396-1400. doi:10.1073/pnas.92.5.1396
[43] Walsh, G., Sexton, D.W., Blaylock, M.G. and Convery, C.M. (1999) Resting and cyto-kine-stimulated human small airway epithelial cells recognize and ingest apoptotic eosinophils. Blood, 94, 2827-2835.
[44] Walsh, G.M. (1999) Advances in the immunobiology of eosinophils and their role in disease. Critical Reviews in Clinical Laboratory Sciences, 36, 453-496. doi:10.1080/10408369991239277
[45] Fadok, V.A., Bratton, D.L., Rose, D.M., Pearson, A., Ezekewitz, R.A.B. and Henson, P.M. (2000) A receptor for phosphatidylserine-specific clearance of apoptotic cells. Nature, 405, 85-90. doi:10.1038/35011084
[46] Fadok, V., Bratton, D.L., Frasch, S.C., Warner, M. and Henson, P.M. (1998) The role of phos-phatidylserine in recognition of apoptotic cells by phagocytes. Cell Death & Differentiation, 5, 551-562. doi:10.1038/sj.cdd.4400404
[47] Fadok, V.A., de Cathelineau, A., Daleke, D.L., Henson, P.M. and Bratton, D.L. (2001) Loss of phospholipid asym- metry and surface exposure of phosphati-dylserine is required for phagocytosis of apoptotic cells by macro- phages and fibroblasts. The Journal of Biological Chemistry, 276, 1071-1077. doi:10.1074/jbc.M003649200
[48] Alenzi, F.Q. (2009) Role of apoptosis in airway epithe- lium. Pakistan Journal of Physiology, 5, 1-10.
[49] Alenzi, F.Q. (2008) Apoptosis and eosinophils. Regula- tion and clinical relevance. Saudi Medical Journal, 29, 643-656.
[50] Alenzi, F.Q., Alenazi, B., Alanzy, F., Mubaraki, A., Salem, M., Al-Jabri, A., Lotfy, M., Bamaga, M., AlRabia, M. and Richard, K.H. (2010) The role of caspase activation and mitochondrial depolarisation in cultured human apoptotic eosinophils. Saudi Journal of Biological Sciences, 17, 29-36.

Copyright © 2024 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.