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

Abstract

Fractures may decrease lung bacterial clearance because FP suppresses PMN CTX to other chemoattractants via FPR-1/2. Trauma activates NETosis but suppresses maximal NETosis. Fractures decrease lung bacterial clearance by multiple mechanisms. PNA after fractures may reflect damage-associated molecular pattern-mediated suppression of PMN antimicrobial function in the lung.