title: Heat stress and reduced plane of nutrition decreases intestinal integrity and function in pigs.
abstract: Heat stress can compromise intestinal integrity and induce leaky gut in a variety of species. Therefore, the objectives of this study were to determine if heat stress (HS) directly or indirectly (via reduced feed intake) increases intestinal permeability in growing pigs. We hypothesized that an increased heat-load causes physiological alterations to the intestinal epithelium, resulting in compromised barrier integrity and altered intestinal function that contributes to the overall severity of HS-related illness. Crossbred gilts (n=48, 43±4 kg BW) were housed in constant climate controlled rooms in individual pens and exposed to 1) thermal neutral (TN) conditions (20°C, 35-50% humidity) with ad libitum intake, 2) HS conditions (35°C, 20-35% humidity) with ad libitum feed intake, or 3) pair-fed in TN conditions (PFTN) to eliminate confounding effects of dissimilar feed intake. Pigs were sacrificed at 1, 3, or 7 d of environmental exposure and jejunum samples were mounted into modified Ussing chambers for assessment of transepithelial electrical resistance (TER) and intestinal fluorescein isothiocyanate (FITC)-labeled lipopolysaccharide (LPS) permeability (expressed as apparent permeability coefficient, APP). Further, gene and protein markers of intestinal integrity and stress were assessed. Irrespective of d of HS exposure, plasma endotoxin levels increased 45% (P<0.05) in HS compared with TN pigs, while jejunum TER decreased 30% (P<0.05) and LPS APP increased 2-fold (P<0.01). Furthermore, d 7 HS pigs tended (P=0.06) to have increased LPS APP (41%) compared with PFTN controls. Lysozyme and alkaline phosphatase activity decreased (46 and 59%, respectively; P<0.05) over time in HS pigs, while the immune cell marker, myeloperoxidase activity, was increased (P<0.05) in the jejunum at d 3 and 7. These results indicate that both HS and reduced feed intake decrease intestinal integrity and increase endotoxin permeability. We hypothesize that these events may lead to increased inflammation, which might contribute to reduced pig performance during warm summer months.
authors.affiliation: Department of Animal Science, Iowa State University, Ames 50011.
authors.forename: S C
authors.initials: SC
authors.lastname: Pearce
authors.forename: V
authors.initials: V
authors.lastname: Mani
authors.forename: T E
authors.initials: TE
authors.lastname: Weber
authors.forename: R P
authors.initials: RP
authors.lastname: Rhoads
authors.forename: J F
authors.initials: JF
authors.lastname: Patience
authors.forename: L H
authors.initials: LH
authors.lastname: Baumgard
authors.forename: N K
authors.initials: NK
authors.lastname: Gabler
mesh_terms: D000821:Animal Feed; D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D004032:Diet / Q000662:veterinary; D005260:Female; D015971:Gene Expression Regulation, Enzymologic / Q000502:physiology; D006358:Hot Temperature; D007422:Intestines / Q000502:physiology*; D008070:Lipopolysaccharides; D009752:Nutritional Status / Q000502:physiology*; D000254:Sodium-Potassium-Exchanging ATPase / Q000235:genetics / Q000378:metabolism; D013312:Stress, Physiological / Q000502:physiology*; D013552:Swine
chemical_list: D008070:Lipopolysaccharides; D000254:Sodium-Potassium-Exchanging ATPase