Modulation of the Triggering Receptor Expressed on the Myeloid Cell Type 1 Pathway in Murine Septic Shock
Autor: | Marie N. Kolopp-Sarda, Gilbert C. Faure, Fabio Benigni, Frédéric Massin, Bruno Levy, Michele Romano, Nadia Passini, Paola Panina-Bordignon, Sébastien Gibot, Cecilia Buonsanti, Marie C. Béné |
---|---|
Přispěvatelé: | Gibot, S., Buonsanti, C., Massin, F., Romano, M., Kolopp-Sarda, M. -N., Benigni, F., Faure, G. C., Bene, M. -C., Panina-Bordignon, P., Passini, N., Levy, B. |
Rok vydání: | 2006 |
Předmět: |
Lipopolysaccharides
Male Molecular Sequence Data Immunology Biology Nitric Oxide Microbiology Nitric oxide Proinflammatory cytokine Sepsis Mice chemistry.chemical_compound medicine Extracellular Animals Amino Acid Sequence Rats Wistar Receptors Immunologic Receptor Adaptor Proteins Signal Transducing Host Response and Inflammation Mice Inbred BALB C Membrane Glycoproteins Septic shock Hydrogen-Ion Concentration medicine.disease Shock Septic Rats Disease Models Animal Infectious Diseases chemistry Cancer research Parasitology Tumor necrosis factor alpha Signal transduction Signal Transduction |
Zdroj: | Infection and Immunity. 74:2823-2830 |
ISSN: | 1098-5522 0019-9567 |
Popis: | The triggering receptor expressed on myeloid cell type 1 (TREM-1) is a cell surface molecule that has been identified on both human and murine polymorphonuclear neutrophils and mature monocytes. The activation of TREM-1 in the presence of microbial components amplifies the inflammatory response and may be responsible for the hyperresponsiveness observed during the initial stage of sepsis. To investigate the effect of the modulation of the TREM-1 pathway during experimental murine sepsis, we used analogue synthetic peptides derived from the extracellular moiety of TREM-1. The TREM-1 ligand was expressed on both peritoneal and peripheral neutrophils during experimental peritonitis in mice. The TREM-1 peptides inhibited the recognition by TREM-1 of its ligand and protected endotoxinic mice from death. In septic rats, the TREM-1 peptides improved the hemodynamic status, attenuated the development of lactic acidosis, modulated the production of such proinflammatory cytokines as tumor necrosis factor alpha and interleukin-1β, and improved survival. The protective effect of these peptides on arterial pressure could partly be explained by a decreased production of nitric oxide. These data suggest that in vivo modulation of TREM-1 might be a suitable therapeutic tool for the treatment of sepsis. Copyright © 2006, American Society for Microbiology. All Rights Reserved. |
Databáze: | OpenAIRE |
Externí odkaz: |