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.

在呼吸过程中，人类每天呼吸超过10,000升的非无菌空气，从而使某些病原体进入肺泡。有趣的是，肺泡的数量超过了肺泡巨噬细胞（AMs），这有利于缺乏AMs的肺泡。如果AM像大多数组织巨噬细胞一样是无柄的，那么除非有来自血液中的中性粒细胞介入，否则病原体将利用这种数字优势。但是，这将导致无处不在的持续性炎症。显影体内肺泡的实时活体成像揭示的AM中，并使用孔科恩的肺泡之间爬行。重要的是，这些巨噬细胞被感测，趋化，高效吞噬吞噬的吸入细菌病原体，例如铜绿假单胞菌和金黄色葡萄球菌。掩盖中性粒细胞中的细菌。AM对细菌的趋化性受损会导致多余的中性粒细胞募集，从而导致不适当的炎症和损伤。在疾病中，甲型流感病毒感染会通过II型干扰素信号传导途径阻碍AM爬行，这大大增加了继发性细菌共感染。