Ryan Rita M, Ahmed Qadeer, Lakshminrusimha Satyan
Division of Neonatology, Department of Pediatrics, Center for Developmental Biology of the Lung, State University of New York at Buffalo, Buffalo, NY, USA.
Clin Rev Allergy Immunol. 2008 Apr;34(2):174-90. doi: 10.1007/s12016-007-8031-4.
Inflammation is important in the development of bronchopulmonary dysplasia (BPD). Polymorphonuclear cells and macrophages and proinflammatory cytokines/chemokines denote early inflammation in clinical scenarios such as in utero inflammation with chorioamnionitis or initial lung injury associated with respiratory distress syndrome or ventilator-induced lung injury. The persistence and non-resolution of lung inflammation contributes greatly to BPD, including altering the lung's ability to repair, contributing to fibrosis, and inhibiting secondary septation, alveolarization, and normal vascular development. Further understanding of the role of inflammation in the pathogenesis of BPD, in particular, during the chronic inflammatory period, offers us the opportunity to develop inflammation-related prevention and treatment strategies of this disease that has long-standing consequences for very premature infants.
炎症在支气管肺发育不良（BPD）的发生发展中起重要作用。多形核细胞、巨噬细胞以及促炎细胞因子/趋化因子代表临床情况下的早期炎症，如伴有绒毛膜羊膜炎的宫内炎症或与呼吸窘迫综合征或呼吸机诱导性肺损伤相关的初始肺损伤。肺部炎症的持续存在和未消退在很大程度上导致了BPD，包括改变肺的修复能力、促成纤维化以及抑制继发性间隔形成、肺泡化和正常血管发育。进一步了解炎症在BPD发病机制中的作用，特别是在慢性炎症期的作用，为我们提供了开发针对这种对极早产儿有长期影响的疾病的炎症相关预防和治疗策略的机会。
