title: Effects of thermal environment on response to acute peripheral lipopolysaccharide challenge exposure in neonatal pigs.
abstract: OBJECTIVE
  To evaluate effects of thermal environment on response to acute peripheral lipopolysaccharide (LPS) challenge exposure in neonatal pigs.
  
  
  METHODS
  26 neonatal pigs.
  
  
  METHODS
  Pigs were assigned to the following treatment groups: 1 warm environment/LPS; 2 warm environment/saline solution; 3 cool environment/LPS; and 4 cool environment/saline solution. For each pig given LPS, 1 littermate of the same sex was given saline solution. Sows with baby pigs were housed in a warm (32 C) or cool (21 C) thermal environment. At 28 days of age, pigs were given 150 micrograms/kg of body weight of Escherichia coli LPS or saline solution intraperitonealy as a control. Rectal temperature and signs of sickness were monitored for 3 hours after LPS administration, when pigs were euthanatized and blood samples were collected to determine serum concentrations of tumor necrosis factor (TNF) alpha and cortisol. To determine in vitro production of TNF alpha, alveolar macrophages were collected by tracheal lavage and incubated for 24 hours at 37 or 41 C, with or without LPS (10 micrograms/ml).
  
  
  RESULTS
  Thermal environment had a significant (P = 0.0004) effect on rectal temperature; LPS administration induced a febrile response (P = 0.0007) only in pigs in the warm environment. All LPS-injected pigs developed signs of endotoxemia; serum TNF alpha and cortisol concentrations were significantly increased (TNF alpha, P = 0.003; cortisol, P = 0.0001); there was no significant in vivo thermal effect on serum TNF alpha and cortisol concentrations. LPS-stimulated alveolar macrophages produced significantly less (P = 0.0086) TNF alpha when incubated at 41 C.
  
  
  CONCLUSIONS
  Thermal environment can have a significant impact on the response of neonatal pigs exposed to bacterial endotoxins.
authors.affiliation: Animal Physiology Unit, United States Department of Agriculture, University of Missouri, Columbia 65211, USA.
authors.forename: J J
authors.initials: JJ
authors.lastname: Klir
authors.forename: L M
authors.initials: LM
authors.lastname: Shahbazian
authors.forename: R L
authors.initials: RL
authors.lastname: Matteri
authors.forename: K L
authors.initials: KL
authors.lastname: Fritsche
authors.forename: B A
authors.initials: BA
authors.lastname: Becker
mesh_terms: D000210:Acute-Phase Reaction / Q000503:physiopathology; D000818:Animals; D000831:Animals, Newborn / Q000097:blood / Q000502:physiology*; D001522:Behavior, Animal / Q000187:drug effects / Q000502:physiology; D001831:Body Temperature / Q000187:drug effects / Q000502:physiology; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D004777:Environment; D004926:Escherichia coli / Q000378:metabolism; D005260:Female; D006358:Hot Temperature; D006854:Hydrocortisone / Q000097:blood / Q000378:metabolism; D008070:Lipopolysaccharides / Q000378:metabolism / Q000494:pharmacology*; D016676:Macrophages, Alveolar / Q000166:cytology / Q000378:metabolism; D008297:Male; D011863:Radioimmunoassay / Q000379:methods / Q000662:veterinary; D011897:Random Allocation; D013552:Swine / Q000097:blood / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000378:metabolism
chemical_list: D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D006854:Hydrocortisone