Regulation of the inflammatory response in asthma by mast cell products

Immunology and Cell Biology - Tập 79 Số 2 - Trang 149-153 - 2001
Prue H. Hart1
1Department of Microbiology and Infectious Diseases, School of Medicine, Flinders University, Adelaide, South Australia, Australia.

Tóm tắt

In airways, mast cells lie adjacent to nerves, blood vessels and lymphatics, which highlights their pivotal importance in regulating allergic inflammatory processes. In asthma, mast cells are predominantly activated by IgE receptor cross linking. In response to activation, preformed mediators that are stored bound to proteoglycans, for example, TNF‐α, IL‐4, IL‐13, histamine, tryptase and chymase, are released. New synthesis of arachidonic acid metabolites (leukotriene C4 (LTC4), leukotriene B4 (LTB4) and prostaglandin D2 (PGD2)) and further cytokines is stimulated. Mediators from degranulating mast cells are critical to the pathology of the asthmatic lung. Mast cell proteases stimulate tissue remodelling, neuropeptide inactivation and enhanced mucus secretion. Histamine stimulates smooth muscle cell contraction, vasodilatation and increased venular permeability and further mucus secretion. Histamine induces IL‐16 production by CD8+ cells and airway epithelial cells; IL‐16 is an important early chemotactic factor for CD4+ lymphocytes. LTC4, LTB4 and PGD2 affect venular permeability and can regulate the activation of immune cells. The best characterized mast cell cytokine in asthmatic inflammation is TNF‐α, which induces adhesion molecules on endothelial cells and subsequent transmigration of inflammatory leucocytes. IL‐13 is critical to development of allergic asthma, although its mode of action is less clear.

Từ khóa


Tài liệu tham khảo

Weidner N, 1990, Evidence for morphologic diversity of human mast cells: an ultrastructural study of mast cells from multiple body sites, Lab. Invest., 63, 63

10.1046/j.1365-2222.1998.00393.x

10.1016/0952-7915(90)90002-X

10.1111/j.1365-2222.1995.tb01024.x

Forsythe P, 1996, Adenosine mediated histamine release from human bronchoalveolar lavage mast cells, Am. J. Respir. Crit. Care Med., 153, A211

Hogaboam C, 1998, Novel role of transmembrane SCF for mast cell activation and eotaxin production in mast cell–fibroblast interactions, J. Immunol., 160, 6166, 10.4049/jimmunol.160.12.6166

Galli SJ, 1993, The c‐kit receptor, stem cell factor, and mast cells, what each is teaching us about the others, Am. J. Pathol., 142, 965

10.1182/blood.V90.11.4438

10.1084/jem.157.6.1981

10.1164/ajrccm/141.4_Pt_1.960

10.1002/jlb.61.3.233

10.1016/S0091-6749(00)90056-3

Denburg JA, 1998, Basophils and mast cells in airway inflammation and asthma, Can. Respir. J., 5, 41A

10.1016/S0091-6749(00)90055-1

10.4049/jimmunol.164.6.2964

10.1016/S0091-6749(05)80223-4

10.1046/j.1365-2222.2000.00100.x

10.1016/S0091-6749(98)70403-8

Rocklin RE, 1977, Histamine‐induced suppressor factor (HSF): Effect on migration inhibitory factor (MIF) production and proliferation, J. Immunol., 118, 1734, 10.4049/jimmunol.118.5.1734

10.1046/j.1365-2249.1997.3791276.x

10.1046/j.1365-2567.1997.00284.x

10.1165/ajrcmb.17.2.2722

Elenkov IJ, 1998, Histamine potently suppresses human IL‐12 and stimulates IL‐10 production via H2 receptors, J. Immunol., 161, 2586, 10.4049/jimmunol.161.5.2586

10.1084/jem.182.1.197

10.1165/ajrcmb.14.5.8624251

10.1023/A:1020531322556

10.1084/jem.184.4.1483

10.1165/ajrcmb.10.5.8179909

10.1073/pnas.86.22.8972

Cumberbatch M, 1994, Modulation of epidermal Langerhans’ cell frequency by tumor necrosis factor‐α, Immunology, 81, 395

Coward WR, 1998, Asthma, adenosine mast cells and theophylline, Clin. Exp. Allergy, 28, 42

10.1146/annurev.iy.07.040189.001045

10.1165/ajrcmb/8.4.349

10.1046/j.1365-2222.1998.00377.x

10.1126/science.282.5397.2258

10.1126/science.282.5397.2261

10.1002/(SICI)1521-4141(199812)28:12<4286::AID-IMMU4286>3.0.CO;2-H

10.1002/jlb.63.6.746

10.1159/000237022

10.1159/000024055

10.1016/B978-012079027-2/50121-0

10.1027/0838-1925.11.3.86

10.1111/j.1398-9995.1998.tb04946.x