Modulation of the triggering receptor expressed on myeloid cells–1 pathway during pneumonia in rats

S Gibot, C Alauzet, F Massin… - The Journal of …, 2006 - academic.oup.com
S Gibot, C Alauzet, F Massin, N Sennoune, GC Faure, MC Béné, A Lozniewski, PE Bollaert…
The Journal of infectious diseases, 2006academic.oup.com
Background Triggering receptor expressed on myeloid cells–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. The aim of the present
study was to investigate the effect of the modulation of the TREM-1 pathway during …
Abstract
BackgroundTriggering receptor expressed on myeloid cells–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. The aim of the present study was to investigate the effect of the modulation of the TREM-1 pathway during experimental pneumonia in rats
MethodsAdult male Wistar rats were intratracheally inoculated with Pseudomonas aeruginosa (PAO1 strain) and randomly treated or not treated with an analogue synthetic peptide derived from the extracellular moiety of TREM-1 (LP17)
Results P. aeruginosa induced a severe pneumonia associated with signs of severe sepsis within the first 24 h. In septic rats, LP17 improved hemodynamic status, attenuated the development of lactic acidosis and hypoxemia, modulated lung and systemic inflammatory responses and coagulation activation, reduced lung histological damage, and improved survival
ConclusionsThe modulation of the TREM-1 pathway by the use of such synthetic peptides as LP17 appears beneficial during P. aeruginosa pneumonia in rats in attenuating lung and systemic inflammatory responses
Oxford University Press