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. 2020 Feb 11;11:91. doi: 10.3389/fimmu.2020.00091

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Copyright © 2020 Sharma, Feng, Britto and Dela Cruz.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Pathogen mechanisms to circumvent direct killing of bacteria by lung epithelial cells. (1) Epithelial cells possess phagocytic ability. (2) Bacteria harbor structures to evade epithelial phagocytosis, such as capsular polysaccharides of Klebsiella pneumoniae. (3) Altered phenotypes in pathogens cause chronic infections e.g., small colony variant of Staphylococcus aureus. (4) Pathogens can live inside the lung epithelium e.g., Bordetella or Legionella. (5) Epithelium releases antimicrobial peptides during lung infections, which bind to the pathogen surface and neutralize the pathogen. (6) During inflammation, a large number of proteins are accumulated in the lung. AMPs interact with other proteins and lose their antimicrobial potency. (7) P. aeruginosa elastase breaks down human LL37 in a dose dependent manner. (8) Pathogen recruited neutrophils contribute to the acidity. SPLUNC loses its function in an acidic environment; also, neutrophil elastases can break down SPLUNC. AMPs, antimicrobial proteins and peptides; SPLUNC, short palate lung and nasal epithelium clone 1.