Lazarus S C
Am J Med. 1986 Nov 14;81(5A):2-7. doi: 10.1016/0002-9343(86)90454-7.
Recent evidence suggests that airway inflammation is linked to hyper-responsiveness of airway smooth muscle. Increases in airway responsiveness after many stimuli are accompanied by increases in inflammatory cells in bronchoalveolar lavage fluid and in the airway epithelium. Airway epithelial cells may themselves be an important source of inflammatory mediators, producing metabolites that can cause chemotaxis of neutrophils and that can selectively activate other cells in the lungs. Mast cells produce a variety of enzymes and vasoactive, chemotactic, and bronchoconstrictor substances in response to non-immunologic as well as immunologic stimuli. The secretory profile of a mast cell may depend upon the specific stimulus applied. In addition, different populations of mast cells exist and distinct enzymatic pathways may predominate in different cell types. Mediators released by these cells may activate target cells by direct or indirect mechanisms. These inflammatory mediators, together with inflammatory cells, are important in the complex interactions involving airway epithelial cells, neutrophils, mast cells, smooth muscle, respiratory secretory cells, and nerves, which, in concert, are responsible for the pathophysiologic manifestations of obstructive lung disease.
最近的证据表明，气道炎症与气道平滑肌的高反应性有关。许多刺激后气道反应性增加的同时，支气管肺泡灌洗液和气道上皮中的炎症细胞也会增加。气道上皮细胞本身可能是炎症介质的重要来源，可产生能引起中性粒细胞趋化并能选择性激活肺内其他细胞的代谢产物。肥大细胞会对非免疫性以及免疫性刺激作出反应，产生多种酶以及血管活性、趋化和支气管收缩物质。肥大细胞的分泌特征可能取决于所施加的特定刺激。此外，存在不同类型的肥大细胞，不同的细胞类型可能以不同的酶促途径为主。这些细胞释放的介质可能通过直接或间接机制激活靶细胞。这些炎症介质与炎症细胞一起，在涉及气道上皮细胞、中性粒细胞、肥大细胞、平滑肌、呼吸道分泌细胞和神经的复杂相互作用中起重要作用，这些因素共同导致阻塞性肺疾病的病理生理表现。
