title: Effect of pretreatment with interleukin-1 beta on inflammatory infiltrates and tissue damage after experimental endotoxic challenge.
abstract: OBJECTIVE
  To evaluate the effect of treatment with murine recombinant interleukin-1 beta on inflammatory infiltrate and tissue damage after experimental endotoxic challenge.
  
  
  METHODS
  Randomized, controlled study.
  
  
  METHODS
  Experimental Unit, Virgen de las Nieves University Hospital.
  
  
  METHODS
  Seventy-two female CBA/H mice, 20-21 g, supplied by the animal center of the Experimental Unit.
  
  
  METHODS
  The mice were randomized into three groups of 24. Group 1 (sham) received two intraperitoneal doses of 0.1 mL of phosphate-buffered saline; group 2 (lipopolysaccharide) was injected with 125 mg/kg lipopolysaccharide (Escherichia coli, intraperitoneally) 24 hrs after 0.1 mL of phosphate-buffered saline; group 3 was pretreated with 80 ng of recombinant interleukin-1 beta per mouse (intraperitoneally) 24 hrs before the endotoxic challenge.
  
  
  RESULTS
  At 1, 2, 4, and 24 hrs after the endotoxic challenge, we studied inflammatory infiltrate and tissue damage in lung, liver, and intestine by determining myeloperoxidase and malondialdehyde tissue concentrations. When we compared the pretreated group with the lipopolysaccharide group, myeloperoxidase concentrations decreased significantly in lung (p <.001) and liver (p <.001) at all study times, and in intestine (p <.001) at 2, 4, and 24 hrs; malondialdehyde concentrations significantly decreased in lung at 1 (p <.05), 2 (p <.01), and 24 (p <.001) hrs, in liver at 2 (p <.001), 4 (p <.01), and 24 (p <.001) hrs, and in intestine at 1 (p <.001), 2, 4 (p <.05), and 24 (p <.001) hrs.
  
  
  CONCLUSIONS
  Pretreatment with recombinant interleukin-1 beta significantly reduces inflammatory infiltrate and tissue damage in mouse lung, liver, and intestine after an experimental endotoxic challenge.
authors.affiliation: Microbiology Department, School of Medicine, University of Los Andes, Mérida, Venezuela.
authors.forename: Luis
authors.initials: L
authors.lastname: Téllez-Gil
authors.forename: Alfonso
authors.initials: A
authors.lastname: Mansilla-Roselló
authors.forename: Antonia
authors.initials: A
authors.lastname: Collado-Torres
authors.forename: Jesús
authors.initials: J
authors.lastname: Villar-del-Moral
authors.forename: Daniel
authors.initials: D
authors.lastname: Garrote-Lara
authors.forename: Trinidad
authors.initials: T
authors.lastname: Villegas-Herrera
authors.forename: María-Jesús
authors.initials: MJ
authors.lastname: Alvarez-Martín
authors.forename: José-Antonio
authors.initials: JA
authors.lastname: Ferrón-Orihuela
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D004731:Endotoxins / Q000494:pharmacology*; D005260:Female; D007375:Interleukin-1 / Q000627:therapeutic use*; D015227:Lipid Peroxidation / Q000187:drug effects; D008070:Lipopolysaccharides / Q000494:pharmacology; D008168:Lung / Q000098:blood supply / Q000201:enzymology / Q000378:metabolism; D008315:Malondialdehyde / Q000097:blood; D051379:Mice; D008808:Mice, Inbred CBA; D009195:Peroxidase / Q000032:analysis / Q000097:blood / Q000187:drug effects; D011014:Pneumonia / Q000097:blood / Q000188:drug therapy* / Q000401:mortality; D016019:Survival Analysis; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D004731:Endotoxins; D007375:Interleukin-1; D008070:Lipopolysaccharides; D008315:Malondialdehyde; D009195:Peroxidase