Mitochondrial damage-associated molecular patterns from fractures suppress pulmonary immune responses via formyl peptide receptors 1 and 2

The Journal of Trauma and Acute Care Surgery
Haipeng LiC J Hauser

Abstract

No known biologic mechanisms link tissue injury with pneumonia (PNA). Neutrophils (PMNs) are innate immune cells that clear bacteria from the lung by migration toward chemoattractants and killing bacteria in neutrophil extracellular traps (NETs). We predicted that tissue injury would suppress PMN antimicrobial function in the lung. We have also shown that mitochondria-derived damage-associated molecular pattern molecules from the bone can alter PMN phenotype and so hypothesized that formyl peptides (FPs) from fractures predispose to PNA by suppressing PMN activity in the lung. Animal studies involved the following. (1) Rats were divided into three groups (10 per condition) as follows: (a) saline injection in the thigh (b) Staphylococcus aureus (SA, 3 × 10) injected intratracheally, or (c) pseudofracture (PsFx; bone supernatant injected in the thigh) plus intratracheally injected SA. (2) Rats were divided into four groups as follows: (a) control, (b) pulmonary contusion (PC), (c) PsFx, and (d) PC + PsFx. Bronchoalveolar lavage was performed 16 hours later. Clinical studies involved the following. (3) Human bone supernatant was assayed for its FP-receptor (FPR) stimulation. (4) Trauma patients' PMN (n = 32; mean ± SE Injury Sever...Continue Reading

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Citations

Nov 26, 2015·Frontiers in Neurology·Jon HazeldineAntonio Belli
Aug 18, 2016·Frontiers in Immunology·Camilla F WenceslauR Clinton Webb
Mar 7, 2018·Nature Immunology·Markus Huber-LangPeter A Ward
May 23, 2018·The Journal of Trauma and Acute Care Surgery·Elzbieta KaczmarekKiyoshi Itagaki
Apr 22, 2017·The Journal of Trauma and Acute Care Surgery·Kiyoshi ItagakiCarl J Hauser
Jun 1, 2018·Journal of Immunology Research·A KovtunA Ignatius
Apr 24, 2021·Proceedings of the National Academy of Sciences of the United States of America·Woon Yong KwonCarl J Hauser

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