James H. Shelhamer; Stewart J. Levine; Tong Wu; David B. Jacoby; Michael A. Kaliner; Stephen I. Rennard
Diseases characterized by airway inflammation, excessive airway secretion, and airway obstruction affect a substantial proportion of the population.These diseases include asthma, chronic bronchitis, bronchiectasis, and cystic fibrosis. Asthma and chronic bronchitis may affect 25 million persons in the United States. Much progress has been made in the last decade toward an understanding of the mechanisms underlying chronic airway inflammation; recent work has resulted in several new concepts of the initiation and maintenance of airway inflammation. Airway production of chemokines, cytokines, and growth factors in response to irritants, infectious agents, and inflammatory mediators may play an important role in the modulation of acute and chronic airway inflammation. Lipid mediators may be produced by resident airway cells and by inflammatory cells; production of these mediators may also be altered by inflammatory cytokines. Increased airway obstruction may be related to intercurrent viral respiratory infection and to the induction of airway inflammation and airway hyperreactivity that results from such infection. Furthermore, several models exist to explain the processes by which airway inflammation is perpetuated in diseases such as asthma and chronic bronchitis. These include neurogenic inflammation, the perpetuation of the acute inflammatory response, and cycles of airway epithelial cell-mediated and inflammatory cell-mediated recruitment and activation of inflammatory cells. An understanding of these mechanisms of airway inflammation may provide the clinician with new therapeutic approaches to the treatment of these common and chronic diseases.
AA = arachidonic acid and metabolites; NEP = neutral endopeptidase; VIP = vasoactive intestinal peptide.
GM-CSF = granulocyte macrophage colony-stimulating factor; iC3b = fragment of the third component of complement; IL-8 = interleukin-8; LTB4 = leukotriene B4.
cPLA2 = cytosolic phospholipase A ; D.C. = dendritic cell; G-CSF = granulocyte colony-stimulating factor; GM-CSF = granulocyte macrophage colony-stimulating factor; HETE = hydroxyeicosatetraenoic acid; ICAM-1 = intercellular adhesion molecule-1; IL-1 = interleukin-1; IL-6 = interleukin-6; IL-8 = interleukin-8; LPS = lipopolysaccharide; LTB4 = leukotriene B4; M = macrophage; MCP-1 = monocyte chemoattractant protein-1; PAF =platelet-activating factor; PMN = neutrophil; T.C. = T lymphocyte; TNF = tumor necrosis factor; VCAM-1 = vascular cell adhesion molecule-1.
B.C. = B lymphocyte; Eos. = eosinophil; 15 LO = 15-lipoxygenase; Hist. = histamine; IL-3 = interleukin-3; IL-4 = interleukin-4; IL-5 = interleukin-5; LCF = lymphocyte colony-stimulating factor; L.N. = lymph node; LTC4/D4 = leukotrienes C4 and D4; M.C. = mast cell; Th-2 = T lymphocyte of the T phenotype.
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Shelhamer JH, Levine SJ, Wu T, Jacoby DB, Kaliner MA, Rennard SI. Airway Inflammation. Ann Intern Med. 1995;123:288–304. doi: 10.7326/0003-4819-123-4-199508150-00008
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Published: Ann Intern Med. 1995;123(4):288-304.
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Print ISSN: 0003-4819 | Online ISSN: 1539-3704
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