title: Temporal pattern and effect of sex on lipopolysaccharide-induced stress hormone and cytokine response in pigs.
abstract: The temporal pattern and sex effect of immune and stress hormone responses to a lipopolysaccharide (LPS) challenge were assessed using a pig model. Secretion of the pro-inflammatory cytokines tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6 increased in a time-dependent manner following LPS infusion. There was also a time-dependent increase in secretion of the stress-related hormones cortisol, epinephrine (E), and norepinephrine (NE) following LPS, with peak concentrations attained within 30 min. The magnitude of the TNF-alpha and IL-1beta responses were both positively associated (P < 0.05) with the magnitude of cortisol response following LPS, whereas serum IL-1beta and IL-6 were positively correlated with the magnitude of E and NE responses following LPS. Acute-phase protein production was also time-dependently increased following LPS. The concentration of immune cells in circulation was decreased (P < 0.05) at 5.5h post-LPS and negatively correlated with pro-inflammatory cytokine production. By 24h post-LPS, immune cell counts increased (P < 0.05) and were positively associated with both pro-inflammatory cytokine and stress hormone production. The amplitude of pro-inflammatory cytokine response following LPS was affected (P < 0.05) by sex classification; however, the magnitude of elevated cytokine concentrations was not. The magnitude of the NE response, but not of the E and cortisol responses, to LPS was influenced by sex (P < 0.05). Similar to the pro-inflammatory cytokines, the magnitude of exposure to the stress hormones following LPS was not influenced by sex. The production of serum amyloid A (SAA) was influenced by sex, with barrows producing more SAA than gilts at 24h post-LPS (P < 0.05). Collectively, these results demonstrate sex-specific, concomitant temporal changes in innate immune- and stress-related hormones.
authors.affiliation: Department of Animal and Wildlife Sciences, College of Agriculture and Human Sciences, Texas A&M University, Kingsville, Texas 78363, USA.
authors.forename: P N
authors.initials: PN
authors.lastname: Williams
authors.forename: C T
authors.initials: CT
authors.lastname: Collier
authors.forename: J A
authors.initials: JA
authors.lastname: Carroll
authors.forename: T H
authors.initials: TH
authors.lastname: Welsh
authors.forename: J C
authors.initials: JC
authors.lastname: Laurenz
mesh_terms: D000818:Animals; D004837:Epinephrine / Q000097:blood / Q000276:immunology; D005260:Female; D006854:Hydrocortisone / Q000097:blood / Q000276:immunology; D007113:Immunity, Innate / Q000276:immunology; D053583:Interleukin-1beta / Q000097:blood / Q000276:immunology; D015850:Interleukin-6 / Q000097:blood / Q000276:immunology; D008070:Lipopolysaccharides / Q000276:immunology / Q000494:pharmacology*; D008297:Male; D009638:Norepinephrine / Q000097:blood / Q000276:immunology; D000685:Serum Amyloid A Protein / Q000032:analysis / Q000276:immunology; D012737:Sex Factors; D013312:Stress, Physiological / Q000276:immunology*; D013552:Swine / Q000097:blood / Q000276:immunology*; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000276:immunology
chemical_list: D053583:Interleukin-1beta; D015850:Interleukin-6; D008070:Lipopolysaccharides; D000685:Serum Amyloid A Protein; D014409:Tumor Necrosis Factor-alpha; D006854:Hydrocortisone; D009638:Norepinephrine; D004837:Epinephrine