Abstract
The pathological mechanisms of gastrointestinal disorders, including inflammatory bowel disease (IBD), in pigs are poorly understood. We report the induction of intestinal inflammation in heat-stressed (HS) pigs, fecal microbiota transplantation from pigs to mice, and explain the role of microorganisms in IBD. 24 adult pigs were subjected to HS (34 ± 1 °C; 75–85% relative humidity for 24h) while 24 control pigs (CP) were kept at 25 ± 3°C and the same humidity. Pigs were sacrificed on days 1, 7, 14, 21. Colonic content microbiome analyses were conducted. Pseudo-germ-free mice were fed by gavage with fecal microbiota from HS-pigs and CP to induce pig-like responses in mice. From 7 d, HS-pigs exhibited fever and diarrhea, and significantly lower colonic mucosal thickness, crypt depth/width, and goblet cell number. Compared with each control group, the concentration of cortisol in the peripheral blood of HS pigs gradually increased, significantly so on days 7, 14, and 21 (P < 0.01). While the concentration of LPS in HS pigs' peripheral blood was significantly higher on days 7, 14 (P < 0.01), and 21 (P < 0.05) compared with that of the control group. The colonic microbiome composition of HS-pigs was different to that of CP. By day 14, opportunistic pathogens (e.g., Campylobacterales) had increased in HS-pigs. The composition of the colonic microbiome in mice administered feces from HS-pigs was different from those receiving CP feces. Bacteroides were significantly diminished, Akkermansia were significantly increased, and intestinal damage and goblet cell numbers were higher in mice that received HS-pig feces. Moreover, we verified the relevance of differences in the microbiota of the colon among treatments. Heat stress promotes changes in gut microbiome composition, which can affect the colonic microbial structure of mice through fecal microbiota transplantation; the molecular mechanisms require further investigation. This study enhanced our understanding of stress-induced inflammation in the colon and the increase in diarrhea in mammals subjected to prolonged HS. Our results provide useful information for preventing or ameliorating deficits in pig production caused by prolonged exposure to high temperatures.
Highlights
Heat stress (HS) refers to heat received in excess of that which the body can tolerate, without physiological impairment
The Diarrhea Index (DI) for the control group was
In the HS group, diarrhea was observed on day 7 and gradually increased thereafter
Summary
Heat stress (HS) refers to heat received in excess of that which the body can tolerate, without physiological impairment. Pigs are more sensitive to HS, compared to other livestock animals, because they produce high metabolic heat, there is quick fat deposition, and lack of functional sweat glands [2]. HS conditions in pigs decrease the food intake, body weight (BW) gain, and meat quality. These together can cause severe losses, as has been evident for the US swine industry, which lost over $300 million annually to HS in 2010 [3]. HS response can markedly reduce post-absorption of carbohydrate, lipid, and protein metabolism in pigs independently of reduced feed intake [4–6], which were associated with intestinal hyperpermeability and swine reproduction [7]. HS decreased the skeletal muscle fatty acid oxidation and metabolic flexibility in pigs [10]
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