Jansen H M, Sachs A P, van Alphen L
Department of Pulmonology, University of Amsterdam, The Netherlands.
Am J Respir Crit Care Med. 1995 Jun;151(6):2073-80. doi: 10.1164/ajrccm.151.6.7767560.
In normal airways, invasion of small numbers of pathogenic bacteria will not give rise to injury or local colonization. In chronic obstructive pulmonary disease, however, local conditions are changed, which may impair local defense systems and facilitate infection. These include: (1) factors promoting bacterial adherence and growth like the observed damaged airway epithelium in chronic bronchitis. The consequent changes in the composition of the epithelial lining fluid and impaired mucociliary clearance may be the most important pathophysiologic airway sequele in this respect; (2) aggravating generalized airway obstruction including mucus secretion, increase in mucus viscosity, and proliferation of submucosal smooth muscles, resulting in significant changes in airway geometry. This may change local conditions dramatically and so sustain factors promoting bacterial infections; (3) subversion of normally protective defense mechanisms into damaging host tissue at the mucosal level. Activated epithelial cell layers induce increased submucosal vascular leakage, edema, and inflammatory cell infiltration with subsequent tissue injury by locally produced cell products like free elastase. Specific bacterial products but also generally produced bacterial endotoxins may induce a local immune response resulting in the local production of high concentrations of antibodies and an invasion of specific effector cells. The role of these reactive cells or proteins may even be a primary one, in that they attack on (cellular) proteins, which increase their susceptibility for dysfunction in the defense line. For the clinicians, the new insights in the role of these aggravating factors in the development of recurrent bacterial airway infections in chronic bronchitis may be of major importance.(ABSTRACT TRUNCATED AT 250 WORDS)
在正常气道中,少量病原菌的侵入不会导致损伤或局部定植。然而,在慢性阻塞性肺疾病中,局部状况发生改变,这可能损害局部防御系统并促进感染。这些因素包括:(1)促进细菌黏附和生长的因素,如在慢性支气管炎中观察到的气道上皮受损。上皮衬液成分的随之改变以及黏液纤毛清除功能受损可能是这方面最重要的病理生理气道后遗症;(2)加重广泛性气道阻塞,包括黏液分泌增加、黏液黏稠度增加以及黏膜下平滑肌增生,导致气道几何形状发生显著变化。这可能会极大地改变局部状况,从而维持促进细菌感染的因素;(3)正常的保护性防御机制在黏膜水平被颠覆,转变为损害宿主组织。活化的上皮细胞层会导致黏膜下血管渗漏增加、水肿和炎症细胞浸润,随后局部产生的细胞产物如游离弹性蛋白酶会造成组织损伤。特定的细菌产物以及普遍产生的细菌内毒素可能会诱导局部免疫反应,导致局部产生高浓度抗体以及特定效应细胞的侵入。这些反应性细胞或蛋白质的作用甚至可能是主要的,因为它们攻击(细胞)蛋白质,增加了它们在防御线上功能障碍的易感性。对于临床医生来说,这些加重因素在慢性支气管炎复发性细菌性气道感染发展中的作用的新见解可能至关重要。(摘要截选至250字)