气候变化领域集成服务门户(CCPortal): Circulating mitochondrial N-formyl peptides contribute to secondary nosocomial infection in patients with septic shock

CCPortal

DOI	10.1073/pnas.2018538118
	Circulating mitochondrial N-formyl peptides contribute to secondary nosocomial infection in patients with septic shock
	Kwon W.Y.; Suh G.J.; Jung Y.S.; Park S.M.; Oh S.; Kim S.H.; Rum Lee A.; Kim J.Y.; Kim H.; Kim K.A.; Kim Y.; Kim B.C.; Kim T.; Kim K.S.; Itagaki K.; Hauser C.J.
发表日期	2021
ISSN	00278424
卷号	118 期号:17
英文摘要	Secondary infections typically worsen outcomes of patients recovering from septic shock. Neutrophil [polymorphonuclear leukocytes (PMNs)] migration to secondarily inoculated sites may play a key role in inhibiting progression from local bacterial inoculation to secondary infection. Mitochondrial N-formyl peptide (mtFP) occupancy of formyl peptide receptor-1 (FPR1) has been shown to suppress PMN chemotaxis. Therefore, we studied the association between circulating mtFPs and the development of secondary infection in patients with septic shock. We collected clinical data and plasma samples from patients with septic shock admitted to the intensive care unit for longer than 72 h. Impacts of circulating nicotinamide adenine dinucleotide dehydrogenase subunit-6 (ND6) upon clinical outcomes were analyzed. Next, the role of ND6 in PMN chemotaxis was investigated using isolated human PMNs. Studying plasma samples from 97 patients with septic shock, we found that circulating ND6 levels at admission were independently and highly associated with the development of secondary infection (odds ratio = 30.317, 95% CI: 2.904 to 316.407, P = 0.004) and increased 90-d mortality (odds ratio = 1.572, 95% CI: 1.002 to 2.465, P = 0.049). In ex vivo experiments, ND6 pretreatment suppressed FPR1-mediated PMN chemotactic responses to bacterial peptides in the presence of multiple cytokines and chemokines, despite increased nondirectional PMN movements. Circulating mtFPs appear to contribute to the development of secondary infection and increased mortality in patients with septic shock who survive their early hyperinflammatory phase. The increased susceptibility to secondary infection is probably partly mediated by the suppression of FPR1-mediated PMN chemotaxis to secondary infected sites. © 2021 National Academy of Sciences. All rights reserved.
英文关键词	Formyl peptide; Infections; Neutrophils; Nosocomial; Sepsis
语种	英语
来源期刊	Proceedings of the National Academy of Sciences of the United States of America
文献类型	期刊论文
条目标识符	http://gcip.llas.ac.cn/handle/2XKMVOVA/179765
作者单位	Department of Emergency Medicine, Seoul National University College of Medicine, Seoul, 03080, South Korea; Department of Emergency Medicine, Seoul National University Hospital, Seoul, 03080, South Korea; Department of Medicine, Seoul National University College of Medicine, Seoul, 03080, South Korea; Department of Bioengineering and Nano-Bioengineering, Incheon National University, Incheon, 22012, South Korea; Division of Nano-Bioengineering, Incheon National University, Incheon, 22012, South Korea; Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, United States
推荐引用方式 GB/T 7714	Kwon W.Y.,Suh G.J.,Jung Y.S.,et al. Circulating mitochondrial N-formyl peptides contribute to secondary nosocomial infection in patients with septic shock[J],2021,118(17).
APA	Kwon W.Y..,Suh G.J..,Jung Y.S..,Park S.M..,Oh S..,...&Hauser C.J..(2021).Circulating mitochondrial N-formyl peptides contribute to secondary nosocomial infection in patients with septic shock.Proceedings of the National Academy of Sciences of the United States of America,118(17).
MLA	Kwon W.Y.,et al."Circulating mitochondrial N-formyl peptides contribute to secondary nosocomial infection in patients with septic shock".Proceedings of the National Academy of Sciences of the United States of America 118.17(2021).