Circulating mitochondrialN-formyl peptides contribute to secondary nosocomial infection in patients with septic shock
Abstract
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.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Apr 22, 2021
- Source ID
- 10.1073/pnas.2018538118
Entities
People
- A. Rum Lee
- Byoung Choul Kim
- Carl J. Hauser
- Gil Joon Suh
- Hayoung Kim
- Jeong Yeon Kim
- Kiyoshi Itagaki
- Kyung Ah Kim
- Kyung Su Kim
- Seung Min Park
- Subi Oh
- Sung Hee Kim
- Tae Gyun Kim
- Woon Yong Kwon
- Yoon Sun Jung
- Young H. Kim
Organizations
- Congressionally Directed Medical Research Programs
- Harvard Medical School
- Incheon National University
- National Research Foundation of Korea
- Seoul National University
- Seoul National University Hospital