Open AccessCirculating mitochondrialN-formyl peptides contribute to secondary nosocomial infection in patients with septic shock
Author(s) -
Woon Yong Kwon,
Gil Joon Suh,
Young-Seok Jung,
Seung Min Park,
Subi Oh,
Sung Hee Kim,
A. Rum Lee,
Jeong Yeon Kim,
Hayoung Kim,
Kyung-Ah Kim,
Young Kim,
Byoung Choul Kim,
Taegyun Kim,
Kyung Soo Kim,
Kiyoshi Itagaki,
Carl J. Hauser
Publication year - 2021
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.2018538118
Subject(s) - septic shock , chemokine , immunology , medicine , odds ratio , sepsis , chemotaxis , shock (circulatory) , microbiology and biotechnology , immune system , biology , receptor
Significance Septic shock commonly leads to multiorgan injury both directly via tissue inflammation and secondarily via hypoperfusion, but both can result in mitochondrialN -formyl peptide (mtFP) release into the circulation. However, no studies have evaluated the role of circulating mtFPs during septic shock. We found that a relatively high plasma nicotinamide adenine dinucleotide dehydrogenase subunit-6 (the most potent human mtFP) level was independently associated with the development of secondary infection in patients with septic shock and that the increased susceptibility to secondary infection is partly attributed to the suppression of polymorphonuclear leukocyte (PMN) chemotaxis by mtFP occupancy of formyl peptide receptor-1. Incorporation of these findings into therapeutic strategies may improve clinical outcomes in septic shock patients by preventing PMN chemotactic anergy.