The Agonists of Formyl Peptide Receptors Prevent Development of Severe Sepsis after Microbial Infection

Title
The Agonists of Formyl Peptide Receptors Prevent Development of Severe Sepsis after Microbial Infection
Author(s)
백석환김상두[김상두]김윤근[김윤근]이화영[이화영]김유선[김유선]전성규[전성규]송동근[송동근]류성호[류성호]배외식[배외식]
Keywords
VAL-D-MET; SYSTEMIC INFLAMMATORY RESPONSE; PLATELET-ACTIVATING-FACTOR; DOUBLE-BLIND; PHOSPHOINOSITIDE HYDROLYSIS; SUPEROXIDE GENERATION; MULTICENTER TRIAL; INDUCED APOPTOSIS; ANTAGONIST TRIAL; CYTOKINE PROFILE
Issue Date
201010
Publisher
AMER ASSOC IMMUNOLOGISTS
Citation
JOURNAL OF IMMUNOLOGY, v.185, no.7, pp.4302 - 4310
Abstract
Severe sepsis, a principal cause of death in intensive care units, occurs when host immune defenses fail to combat invading microbes. In this paper, we report that the administration of peptide agonists of formyl peptide receptors, including Trp-Lys-Tyr-Met-Val-D-Met (WKYMVm), protected against death by enhanced bactericidal activity and inhibition of vital organ inflammation and immune cell apoptosis in a cecal ligation and puncture (CLP) sepsis mouse model. The administration of WKYMVm also enhanced the production of type 1 (IFN-gamma and IL-12) and type 17 (IL-17 and TGF-beta) cytokines in CLP mice. In contrast, the administration of WKYMVm inhibited the production of proinflammatory cytokines (TNF-alpha, IL-1 beta, and IL-6) in the CLP mice. The therapeutic and bactericidal effects of WKYMVm were partly reversed in IFN-gamma-deficient mice, whereas target organ inflammation was not. Meanwhile, the therapeutic and anti-inflammatory effects of WKYMVm were partly reversed in IL-17-deficient mice. In addition, the administration of WKYMVm also enhanced type 1 and type 17 Th cell responses in mice sensitized with LPS plus Ags. These results suggest that the agonists of formyl peptide receptors effectively prevent development of severe sepsis following microbial infection partly via augmentation of type 1 and type 17 immune responses. The Journal of Immunology, 2010, 185: 4302-4310.
URI
http://hdl.handle.net/YU.REPOSITORY/23533http://dx.doi.org/10.4049/jimmunol.1001310
ISSN
0022-1767
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의과대학 > 생화학.분자생물학교실 > Articles
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