Chronic social stress in pigs impairs intestinal barrier and nutrient transporter function, and alters neuro-immune mediator and receptor expression.
Psychosocial stress is a major factor driving gastrointestinal (GI) pathophysiology and disease susceptibility in humans and animals. The mechanisms governing susceptibility to stress-induced GI disease remain poorly understood. In the present study, we investigated the influence of chronic social stress (CSS) in pigs, induced by 7 d of chronic mixing/crowding stress, on intestinal barrier and nutrient transport function, corticotropin releasing factor (CRF) signaling and immunological responses. Results from this study showed that CSS resulted in a significant impairment of ileal and colonic barrier function indicated by reduced transepithelial electrical resistance (TER) in the ileum and increased FD4 flux in the ileum (by 0.8 fold) and colon (by 0.7 fold). Ileal sodium glucose linked transporter 1 (SGLT-1) function, measured as glucose-induced changes in short-circuit current (Isc), was diminished (by 52%) in CSS pigs, associated with reduced body weight gain and feed efficiency. Although reductions in SGLT-1 function were observed in CSS pigs, mRNA expression for SGLT-1, villus heights were increased in CSS pigs. Corticotropin releasing factor (CRF) mRNA was upregulated (by 0.9 fold) in the ileum of CSS pigs but not in the colon. Urocortin 2 (Ucn2) mRNA was upregulated (by 1.5 fold) in the colon of CSS pigs, but not in the ileum. In CSS pigs, a downregulation of pro-inflammatory cytokines mRNA (IL1B, TNFA, IL8, and IL6) was observed in both ileum and colon, compared with controls. In contrast CSS induced a marked upregulation of mRNA for IL10 and mast cell chymase gene (CMA1) in the ileum and colon. Together, these data demonstrate that chronic stress in pigs results in significant alterations in intestinal barrier and nutrient transport function and neuro-immune mediator and receptor expression.
Gastrointestinal Stress Biology Laboratory, Michigan State University, East Lansing, Michigan, United States of America.|Department of Large Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University, East Lansing, Michigan, United States of America.
Yihang
Y
Li
Zhejiang University, College of Animal Sciences, Hangzhou, P. R. China.
Zehe
Z
Song
Gastrointestinal Stress Biology Laboratory, Michigan State University, East Lansing, Michigan, United States of America.
Katelyn A
KA
Kerr
Gastrointestinal Stress Biology Laboratory, Michigan State University, East Lansing, Michigan, United States of America.|Department of Large Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University, East Lansing, Michigan, United States of America.|Neuroscience Program, Michigan State University, East Lansing, Michigan, United States of America.|Department of Physiology, Michigan State University, East Lansing, Michigan, United States of America.
Adam J
AJ
Moeser
D000818:Animals; D001692:Biological Transport; D015415:Biomarkers; D003106:Colon / Q000378:metabolism; D003346:Corticotropin-Releasing Hormone / Q000235:genetics / Q000378:metabolism; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D015870:Gene Expression; D005947:Glucose / Q000378:metabolism; D006854:Hydrocortisone / Q000097:blood; D007082:Ileum / Q000378:metabolism; D007413:Intestinal Mucosa / Q000276:immunology* / Q000378:metabolism* / Q000473:pathology; D015213:Neuroimmunomodulation / Q000235:genetics / Q000276:immunology; D011956:Receptors, Cell Surface / Q000235:genetics*; D013315:Stress, Psychological; D013552:Swine
D015415:Biomarkers; D016207:Cytokines; D011956:Receptors, Cell Surface; D003346:Corticotropin-Releasing Hormone; D005947:Glucose; D006854:Hydrocortisone