title: Integrated adrenal, somatotropic, and immune responses of growing pigs to treatment with lipopolysaccharide.
abstract: The objective of this research was to provide an integrated look at systemic adrenal, somatotropic, and immune responses of growing pigs to challenge with lipopolysaccharide (LPS). Weaned pigs were challenged intraperitoneally with 100 microg/kg BW of LPS or sterile saline, and rectal temperature and blood data were collected for 72 h. Daily feed intake also was monitored. Plasma was analyzed for concentrations of cortisol, tumor necrosis factor alpha (TNFalpha), the acute phase protein haptoglobin, growth hormone (GH), insulin-like growth factor I (IGF-I), and prostaglandin E2 (PGE2). As expected, LPS decreased feed intake, stimulated a febrile response, and activated the hypothalamic-pituitary-adrenal (HPA) axis as demonstrated by increased cortisol levels. Cortisol reached maximum elevation 2 h after treatment (P < .001) and remained elevated through 12 h (P < .001). Circulating TNFalpha was increased by LPS at 2 and 4 h after treatment (P < .001), and an apparent (not statistically significant) increase in haptoglobin also occurred in challenged animals. The LPS injection suppressed IGF-I by 2 h following treatment (P < .01), and circulating IGF-I remained reduced relative to controls through 44 h. Overall, GH was increased in LPS-treated pigs (P < .05), although the treatment x time interaction was not significant. Plasma PGE2 was increased transiently at 2 h (P < .05) and then subsequently suppressed at 4, 8, and 12 h following LPS (P < .05). This study provides a comprehensive view of systemic effects of LPS on components of the HPA, growth, and immune axes. In addition, these are the first data to document changes in circulating PGE2 in unrestrained animals during the early hours of the acute phase response to LPS.
authors.affiliation: Department of Animal Science and Industry, Kansas State University, Manhattan 66506-0201, USA.
authors.forename: K J
authors.initials: KJ
authors.lastname: Wright
authors.forename: R
authors.initials: R
authors.lastname: Balaji
authors.forename: C M
authors.initials: CM
authors.lastname: Hill
authors.forename: S S
authors.initials: SS
authors.lastname: Dritz
authors.forename: E L
authors.initials: EL
authors.lastname: Knoppel
authors.forename: J E
authors.initials: JE
authors.lastname: Minton
mesh_terms: D000311:Adrenal Glands / Q000187:drug effects*; D000818:Animals; D001831:Body Temperature / Q000187:drug effects; D015232:Dinoprostone / Q000097:blood; D002149:Energy Intake / Q000187:drug effects; D013006:Growth Hormone / Q000097:blood*; D006242:Haptoglobins / Q000032:analysis; D006854:Hydrocortisone / Q000097:blood; D007249:Inflammation / Q000139:chemically induced; D007334:Insulin-Like Growth Factor I / Q000032:analysis*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D013552:Swine / Q000254:growth & development*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D014886:Weaning
chemical_list: D006242:Haptoglobins; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone; D015232:Dinoprostone; D006854:Hydrocortisone