title: Twelve hours of heat stress induces inflammatory signaling in porcine skeletal muscle.
abstract: Heat stress causes morbidity and mortality in humans and animals and threatens food security by limiting livestock productivity. Inflammatory signaling may contribute to heat stress-mediated skeletal muscle dysfunction. Previously, we discovered increased circulating endotoxin and intramuscular oxidative stress and TNF-α protein abundance, but not inflammatory signaling following 24 and 72 h of heat stress. Thus the purpose of this investigation was to clarify the role of inflammatory signaling in heat-stressed skeletal muscle. Crossbred gilts (n = 8/group) were assigned to either thermal neutral (24°C), heat stress (37°C), or pair-fed thermal neutral (24°C) conditions for 12 h. Following treatment, animals were euthanized, and the semitendinosus red (STR) and white (STW) were recovered. Heat stress did not alter inflammatory signaling in STW. In STR, relative heat shock protein abundance was similar between groups, as was nuclear content of heat shock factor 1. In whole homogenate, relative abundance of the NF-κB activator inhibitory κB kinase-α was increased by heat stress, although abundance of NF-κB was similar between groups. Relative abundance of phosphorylated NF-κB was increased by heat stress in nuclear fractions. Activator protein-1 (AP-1) signaling was similar between groups. While there were few differences in transcript expression between thermal neutral and heat stress, 80 and 56% of measured transcripts driven by NF-κB or AP-1, respectively, were increased by heat stress compared with pair-fed thermal neutral. Heat stress also caused a reduction in IL-6 transcript and relative protein abundance. These data demonstrate that short-term heat stress causes inflammatory signaling through NF-κB in oxidative, but not glycolytic, skeletal muscle.
authors.affiliation: Department of Animal Science, Iowa State University, Ames, Iowa; and.
authors.forename: Shanthi
authors.initials: S
authors.lastname: Ganesan
authors.affiliation: Department of Animal Science, Iowa State University, Ames, Iowa; and.
authors.forename: Carmen
authors.initials: C
authors.lastname: Reynolds
authors.affiliation: Department of Animal Science, Iowa State University, Ames, Iowa; and.
authors.forename: Katrin
authors.initials: K
authors.lastname: Hollinger
authors.affiliation: Department of Animal Science, Iowa State University, Ames, Iowa; and.
authors.forename: Sarah C
authors.initials: SC
authors.lastname: Pearce
authors.affiliation: Department of Animal Science, Iowa State University, Ames, Iowa; and.
authors.forename: Nicholas K
authors.initials: NK
authors.lastname: Gabler
authors.affiliation: Department of Animal Science, Iowa State University, Ames, Iowa; and.
authors.forename: Lance H
authors.initials: LH
authors.lastname: Baumgard
authors.affiliation: Department of Animal and Poultry Sciences, Virginia Polytechnic Institute and State University, Blacksburg, Virginia.
authors.forename: Robert P
authors.initials: RP
authors.lastname: Rhoads
authors.affiliation: Department of Animal Science, Iowa State University, Ames, Iowa; and jselsby@iastate.edu.
authors.forename: Joshua T
authors.identifier: 0000-0002-5205-5834
authors.initials: JT
authors.lastname: Selsby
mesh_terms: D000818:Animals; D016207:Cytokines / Q000276:immunology*; D018882:Heat Stress Disorders / Q000276:immunology*; D018869:Heat-Shock Response / Q000276:immunology*; D058847:Inflammasomes / Q000276:immunology; D018836:Inflammation Mediators / Q000276:immunology*; D018482:Muscle, Skeletal / Q000276:immunology*; D009220:Myositis / Q000276:immunology*; D017382:Reactive Oxygen Species / Q000276:immunology; D015398:Signal Transduction / Q000276:immunology; D013552:Swine
chemical_list: D016207:Cytokines; D058847:Inflammasomes; D018836:Inflammation Mediators; D017382:Reactive Oxygen Species
keywords: AP-1; NF-κB; heat stroke; hyperthermia; inflammation