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Heat stressed pigs show typical characteristics of inflammatory bowel disease (IBD). However, little is known about the pathogenesis of heat stress (HS)-induced IBD in pigs. In this study, we determined the effects of HS on colon morphology, intestinal microbiota diversity, transcriptome genes (transcripts), and short chain fatty acids (SCFAs) metabolism in pigs. In addition, the correlation among these parameters was analyzed by weighted gene co-expression network analysis. Results showed that the liver and kidney functions related to blood biochemical indexes were partially changed in pigs under HS. Furthermore, the levels of diamine oxidase and D-lactic acid were significantly increased, whereas the levels of secretory immunoglobulin A were decreased. The integrity of colonic tissue was damaged under HS, as bleeding, lymphatic infiltration, and villi injury were observed. The concentrations of SCFAs in the colon, such as acetic acid and butyric acid, were decreased significantly. In addition, the composition of colon microbiota, such as decrease in Lactobacillus johnsonii, Lactobacillus reuteri and increase in Clostridium sensu stricto 1 of day 7 and 14 while under HS. These changes were associated with changes in the concentration of SCFAs and biochemical indexes above mentioned. Differentially expressed genes were enriched in the nucleotide-binding oligomerization domain-like receptor signaling pathway, Th17 cell differentiation, and IBD pathway, which were also associated with the changes in SCFAs. Thus, the structure, diversity of intestinal microorganisms, and changes in the levels of SCFAs in colon of heat stressed pigs changed significantly, contributing to the activation of immune response and inflammatory signal pathways and causing abnormal physiological and biochemical indexes and intestinal mucosal damage. These results highlight the interconnections between intestinal microbiota, SCFAs, and immune response and their role in the pathogenesis of stress induced IBD therapy.

Heat stress can significantly affect the immune function of the animal body. Heat stress stimulates oxidative stress in intestinal tissue and suppresses the immune responses of mice. The protecting effects of chitosan on heat stress induced colitis have not been reported. Therefore, the aim of this study was to investigate the protective effects of chitosan on immune function in heat stressed mice. Mice were exposed to heat stress (40 °C per day for 4 h) for 14 consecutive days. The mice (C57BL/6J), were randomly divided into three groups including: control group, heat stress, Chitosan group (LD: group 300 mg/kg/day, MD: 600 mg/kg/day, HD: 1000 mg/kg/day). The results showed that tissue histology was improved in chitosan groups than heat stress group. The current study showed that the mice with oral administration of chitosan groups had improved body performance as compared with the heat stress group. The results also showed that in chitosan treated groups the production of HSP70, TLR4, p65, TNF-α, and IL-10 was suppressed on day 1, 7, and 14 as compared to the heat stress group. In addition Claudin-2, and Occludin mRNA levels were upregulated in mice receiving chitosan on day 1, 7, and 14 of heat stress. Furthermore, the IL-6, IL-10, and TNF-α plasma levels were down-regulated on day 1, 7, and 14 of heat stress in mice receiving the oral administration of chitosan. In conclusion, the results showed that chitosan has an anti-inflammatory ability to tolerate hot environmental conditions.

Heat stress has severe implications on the health of mice involving intestinal mucosal barrier damage and dysregulated mucosal immune response. This study was designed with long-term heat stress to detect the protective effect of terpinen4-ol on body weight, colon length, organ index, morphological structure, inflammatory cytokines expression, Claudin-2, Occludin, and TLR4 signaling pathway of colonic tissue in mice under heat stress. A study found that oral administration of terpinen4-ol helped against mortality and intestinal inflammation in a mouse model of acute colitis induced by heat stress (40 °C per day for 4 h) exposed for 14 consecutive days. The mice were divided into five groups including control, heat stress, terpinen4-ol low dose (TER LD: 5 mg/kg), medium dose (TER MD: 10 mg/kg), and high dose (TER HD: 20 mg/kg) group. Our study showed that the heat-stress terpinen4-ol group had improved body weight, colon length, and organ index, the number of white blood cells, lymphocytes, and neutrophils in the blood as compared to the heat stress group. In addition, results showed that heat stress upregulated the expression of TLR4, p65, TNF-α, and IL-10. While, in mice receiving the oral administration of terpinen4-ol, the production of TNF-α, IL-10, TLR4, and p65 was suppressed on day 1, 7, and 14 of heat stress. In addition Claudin-2, Occludin mRNA levels were upregulated in mice receiving terpinen4-ol on day 1, 7, and 14 of heat stress. Furthermore, the IL-6, IL-10, TNF-α serum levels were also upregulated in mice under heat stress, but in mice receiving the oral administration of terpinen4-ol, the IL-6, IL-10, TNF-α level was down-regulated on day 1, 7, and 14 of heat stress. Histomorphological examination found that as compared to the control group, the muscle layer thickness and villi height of mice in the heat stress group were significantly reduced, while the changes of the above indicators in the terpinene4-ol groups were improved than those in the heat stress group. In conclusion, the terpinen4-ol has a protective effect on colonic tissue damage induced by heat stress.