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• W1507163025 endingPage "74" @default.
• W1507163025 startingPage "29" @default.
• W1507163025 abstract "Asthma is characterized by reversible obstruction and hyperreactivity of the airways associated with an inflammatory infiltration by lymphocytes, macrophages, and eosinophils which may induce airway remodeling and permanent lung damage.Mast cells are key players in the allergic response. Activated by antigens cross-linking surface IgE, mast cells release preformed mediators (including histamine and chemotactic factors) and synthesize newly-generated mediators (including LTC4 and PGD2) which induce an early-phase reaction associated with bronchospasm and a late-phase reaction characterized by inflammation. Mast cells also synthesize cytokines, low molecular weight peptides that regulate immune and inflammatory responses.Eosinophils are major effectors of airway damage in asthma, primarily through the release of major basic protein and eosinophil cationic protein, both of which are toxic to airway epithelial cells.T lymphocytes are the primary regulators of the immune response. CD4+ helper T cells may differentiate into Thl cells, which secrete predominantly IL-2 and IFN-g, or Th2 cells, which preferentially secrete IL-4, IL-5, IL-6, IL-10, and IL-13. Thl cytokines promote cytotoxicity, delayed-type hypersensitivity reactions, and monocyte activation, whereas the Th2 cytokines IL-4 and IL-13 induce IgE synthesis and IL-5 activates eosinophils.Monocytes are the principal source of IL-12, which induces IFN-g synthesis and promotes differentiation of Thl cells, but also release IL-10, which inhibits Thl development. In the lungs, monocytes differentiate into alveolar macrophages, which produce nitric oxide and may contribute to airway damage.Airway epithelial and smooth muscle cells actively participate in the allergic response by releasing arachidonic acid metabolites, cytokines, and chemokines, thereby serving both as effector and target cells. The bronchial epithelium is the primary source of the potent bronchoconstrictor endothelin and, with macrophages, accounts for most nitric oxide synthesis in the airways.Cellular adhesion molecules regulate both cell-cell and cell-extracellular matrix protein interactions and are essential for the recruitment of leukocytes to sites of inflammation. Proinflammatory cytokines upregulate the expression of these molecules and thus augment the inflammatory response.Neural control of the airways is mediated through adrenergic (sympathetic), cholinergic (parasympathetic), and nonadrenergic, noncholinergic (NANC) systems. Stimulation of the cholinergic nervous system induces bronchoconstriction and mucus secretion. Neurotransmitters in the NANC system include the excitatory mediators substance P and neurokinin A, which induce bronchoconstriction, and the inhibitory mediators vasoactive intestinal peptide and nitric oxide, both potent bronchodilators." @default.
• W1507163025 created "2016-06-24" @default.
• W1507163025 creator A5032263172 @default.
• W1507163025 creator A5069423887 @default.
• W1507163025 date "2001-01-01" @default.
• W1507163025 modified "2023-09-24" @default.
• W1507163025 title "Pathogenesis of Asthma" @default.
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