Pathogenesis of severe pneumonia: advances and knowledge gaps.
Pathogenesis of severe pneumonia: advances and knowledge gaps.
复制标题
DOI：
10.1097/mcp.0000000000000365
复制
发表时间：
2017-05
影响因子：
3.3
通讯作者：
Mizgerd JP
中科院分区：
文献类型：
--
作者：
Mizgerd JP
肺炎是一种常见疾病，在一部分患者中变得严重，取决于宿主生物学，包括免疫抵抗和组织弹性机制。这篇综述强调了2016年以来肺炎生物学的发现，突出了特别紧迫或新出现的问题和方向。在不同的白细胞亚型之间以及白细胞与肺的结构细胞之间，已经阐明了介导针对肺中微生物的先天免疫应答的新型细胞-细胞相互作用。适应性免疫在确定肺炎的结果方面受到越来越多的关注，特别是由反复既往呼吸道感染和直接异型回忆反应引起的肺驻留记忆细胞。已经确定了新的组织弹性成分，有助于感染肺部的抗炎、促进消退、组织保护和修复再生途径。最近的发现将指导对肺保护的基本机制的研究。从长远来看，操纵这些途径对临床实践有影响，因为增强抵抗力和恢复力的策略有可能改善严重肺炎。
Pneumonia is a common disease that becomes severe in a subset of patients, dependent on host biology including mechanisms of immune resistance and tissue resilience. This review emphasizes discoveries in pneumonia biology from 2016, highlighting questions and directions that are especially pressing or newly emerging. Novel cell-cell interactions mediating innate immune responses against microbes in the lung have been elucidated, between distinct leukocyte sub-types as well as between leukocytes and the structural cells of the lung. Adaptive immunity has received growing attention for determining the outcome of pneumonia, particularly the lung resident memory cells that arise from repeated prior respiratory infections and direct heterotypic recall responses. New tissue resilience components have been identified that contribute to anti-inflammatory, pro-resolution, tissue-protective, and reparative regeneration pathways in the infected lung. Recent findings will direct research into fundamental mechanisms of lung protection. Over the longer term, manipulating these pathways has implications for clinical practice, as strategies to bolster resistance and resilience have potential to ameliorate severe pneumonia.