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

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

JOURNAL OF TRAUMA AND ACUTE CARE SURGERY, cilt.78, sa.2, ss.272-279, 2015 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 78 Sayı: 2
  • Basım Tarihi: 2015
  • Doi Numarası: 10.1097/ta.0000000000000509
  • Dergi Adı: JOURNAL OF TRAUMA AND ACUTE CARE SURGERY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.272-279
  • İstanbul Üniversitesi Adresli: Evet

Özet

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.