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

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Li H., Itagaki K., Sandler N., Gallo D., Galenkamp A., Kaczmarek E., ...More

JOURNAL OF TRAUMA AND ACUTE CARE SURGERY, vol.78, no.2, pp.272-279, 2015 (SCI-Expanded)

• Publication Type: Article / Article
• Volume: 78 Issue: 2
• Publication Date: 2015
• Doi Number: 10.1097/ta.0000000000000509
• Journal Name: JOURNAL OF TRAUMA AND ACUTE CARE SURGERY
• Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
• Page Numbers: pp.272-279
• Istanbul University Affiliated: Yes

Abstract

BACKGROUND: 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.