生物
炎症
微生物学
背景(考古学)
免疫系统
细菌
先天免疫系统
趋化性
细胞生物学
吞噬作用
巨噬细胞
免疫学
体外
古生物学
受体
生物化学
遗传学
作者
Arpan Sharma Neupane,Michelle Willson,Andrew Chojnacki,Fernanda V. S. Castanheira,Christopher Morehouse,Agostina Carestia,Ashley Keller,Moritz Peiseler,Antonio DiGiandomenico,Margaret M. Kelly,Matthias Amrein,Craig N. Jenne,Ajitha Thanabalasuriar,Paul Kubes
出处
期刊:Cell
[Elsevier]
日期:2020-09-03
卷期号:183 (1): 110-125.e11
被引量:195
标识
DOI:10.1016/j.cell.2020.08.020
摘要
During respiration, humans breathe in more than 10,000 liters of non-sterile air daily, allowing some pathogens access to alveoli. Interestingly, alveoli outnumber alveolar macrophages (AMs), which favors alveoli devoid of AMs. If AMs, like most tissue macrophages, are sessile, then this numerical advantage would be exploited by pathogens unless neutrophils from the blood stream intervened. However, this would translate to omnipresent persistent inflammation. Developing in vivo real-time intravital imaging of alveoli revealed AMs crawling in and between alveoli using the pores of Kohn. Importantly, these macrophages sensed, chemotaxed, and, with high efficiency, phagocytosed inhaled bacterial pathogens such as P. aeruginosa and S. aureus, cloaking the bacteria from neutrophils. Impairing AM chemotaxis toward bacteria induced superfluous neutrophil recruitment, leading to inappropriate inflammation and injury. In a disease context, influenza A virus infection impaired AM crawling via the type II interferon signaling pathway, and this greatly increased secondary bacterial co-infection.
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