Fibroblasts proliferate in response to several cytokines and mediators generated during an allergic inflmmatory response. Recognized firoblast mitogens include histamine, heparin, and tryptase derived from mast cells, and major basic protein (MBP) and eosinophil cationic protein (ECP) from eosinophils. The cytokines TGF- β as well as platelet-derived growth factor (PDGF), b-firoblastgrowth factor (b-FGF), insulin-like growth factor 1 (IGF1), IL-1, and endothelin released during chronic allergic inflmmation promote fibroblast proliferation, differetiation, and activation.TGF-β enhances production of a range of extracellular matrix components, and decreases the synthesis of matrix-degrading enzymes while increasing the synthesis of protease inhibitors. Thus, TGF- β promotes the deposition of extracellular matrix while inhibiting its degradation, and contributes to the widespread subepithelial extracellular matrix deposition that may be associated with chronic allergic inflmmation.Chronic allergic inflmmation may lead to the deposition of types III and V ‘repair’ collagens in the lamina reticularis beneath the types IV and VII ‘reticular’ collagens, which largely make up the basement membrane.The altered sub-basement membrane region also contains increased deposition of extracellular matrix components including fironectin, tenascin, and lamin. Myofiroblasts present below the basement membrane are increased in number in asthma and are the source of many of the extracellular matrix products that are expressed after allergen challenge. so as you see the allergy is phenomenon complex ...
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