title: Modulation of the triggering receptor expressed on myeloid cells-1 pathway during pneumonia in rats.
abstract: 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 experimental pneumonia in rats.
  
  
  METHODS
  Adult 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.
  
  
  CONCLUSIONS
  The 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.
authors.affiliation: Service de Réanimation Médicale, Hôpital Central, 54035 Nancy, France. s.gibot@chu-nancy.fr
authors.forename: Sébastien
authors.initials: S
authors.lastname: Gibot
authors.forename: Corentine
authors.initials: C
authors.lastname: Alauzet
authors.forename: Frédéric
authors.initials: F
authors.lastname: Massin
authors.forename: Nassira
authors.initials: N
authors.lastname: Sennoune
authors.forename: Gilbert C
authors.initials: GC
authors.lastname: Faure
authors.forename: Marie-Christine
authors.initials: MC
authors.lastname: Béné
authors.forename: Alain
authors.initials: A
authors.lastname: Lozniewski
authors.forename: Pierre-Edouard
authors.initials: PE
authors.lastname: Bollaert
authors.forename: Bruno
authors.initials: B
authors.lastname: Lévy
mesh_terms: D000595:Amino Acid Sequence; D000818:Animals; D022801:Complementarity Determining Regions / Q000737:chemistry; D004195:Disease Models, Animal; D006801:Humans; D008168:Lung / Q000382:microbiology / Q000473:pathology; D008297:Male; D008562:Membrane Glycoproteins / Q000737:chemistry / Q000378:metabolism*; D051379:Mice; D008969:Molecular Sequence Data; D022423:Myeloid Cells / Q000276:immunology / Q000378:metabolism*; D010455:Peptides / Q000138:chemical synthesis / Q000737:chemistry / Q000494:pharmacology / Q000627:therapeutic use*; D018410:Pneumonia, Bacterial / Q000188:drug therapy* / Q000276:immunology / Q000401:mortality / Q000473:pathology; D011552:Pseudomonas Infections / Q000188:drug therapy / Q000276:immunology / Q000401:mortality / Q000473:pathology; D011550:Pseudomonas aeruginosa / Q000276:immunology / Q000472:pathogenicity; D051381:Rats; D017208:Rats, Wistar; D011971:Receptors, Immunologic / Q000737:chemistry / Q000378:metabolism*; D018805:Sepsis / Q000188:drug therapy / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D016896:Treatment Outcome; D000073871:Triggering Receptor Expressed on Myeloid Cells-1
chemical_list: D022801:Complementarity Determining Regions; D008562:Membrane Glycoproteins; D010455:Peptides; D011971:Receptors, Immunologic; C408842:TREM1 protein, human; D000073871:Triggering Receptor Expressed on Myeloid Cells-1