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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.

Background Various stressors alter the 'brain-gut axis' and contribute to many gastrointestinal disorders such as inflammatory bowel disease. However, the pathological mechanisms of these perturbations are poorly understood. Here, we report on the induction of intestinal inflammation in heat-stressed pigs and apply fecal microbiota transplantation from pigs to mice to elucidate the role of intestinal microbiota in TLR4/NF-κB signaling pathway activation. Results Twelve healthy adult pigs were subjected to heat stress (34 ± 1 °C and 75–85% relative humidity) and compared with 12 control pigs exposed to 25 ± 3 °C and the same humidity level. The pigs were sacrificed on days 1, 7, 14, and 21. Their colonic contents were collected for microbiome analyses and their colonic epithelia underwent transcriptome analyses. Pseudo-germ-free mice were gavaged with fecal bacteria from heat-stressed and control pigs on the collection days to determine whether gut microbiomes and immune responses resembling those in the pigs could be induced in the mice. Heat-stressed pigs presented with fever and diarrhea from day 7 and their colonic villus length, crypt depth/width, and goblet cell number were significantly lower than those of the controls. Their TLR4, TRAF6, and nuclear p65 were upregulated at the RNA and protein levels. Their proinflammatory IL-6, IL-8, and IL-17 were also upregulated. Colonic microflora composition in the heat-stressed pigs markedly differed from that of the controls. By day 14, the former presented with substantial increases in opportunistic pathogens such as Campylobacterales , Veillonellaceae , and Megasphaera . Intestinal lipopolysaccharide concentrations were higher in the heat-stressed than the control pigs. Mice administered fecal transplantation from heat-stressed pigs had a distinctly different colonic microflora composition from those receiving control pig fecal transplantation. Bacteroides were significantly diminished and Akkermansia were significantly augmented in mice administered feces from heat-stressed pigs for 14 d. In the colonic tissues of mice given feces from heat-stressed pigs, the TLR4/NF-κB signaling pathway was activated and there was a mild inflammatory response. Conclusion Heat stress promotes changes in gut microflora composition which, in turn, activates the TLR4/NF-κB signaling pathway and causes inflammatory bowel disease in pigs.

Disease outbreaks heavily impact the economic viability of animal industries. Little is known about the mechanisms of immune system-related diseases in geese. Toll-like receptors (TLRs) play a major role in the anti-inflammatory immunity process in most animal species, but they have not been studied in the Magang goose. To elucidate the role of TLRs, reverse transcription polymerase chain reaction (RT-PCR) and PCR amplification of cDNA ends (Smart RACE) were used to clone the Magang goose TLR5 gene (mgTLR5). The full-length cDNA of mgTLR5 was 2967 bp in length, including a 5'-terminal untranslated region (UTR) of 215 bp, a 3'-terminal UTR of 384 bp, and an open reading frame of 2583 bp that encodes a protein of 860 amino acids. Structurally, mgTLR5 has a toll/interleukin-receptor (TIR) domain, a transmembrane domain, and seven leucine-rich repeats (LRRs) domains. Homology alignment of TLR5 and its TIR domains with other species revealed that mgTLR5 shared 98 % and 81.3 % of sequence similarity with white goose TLR5 and chicken TLR5, respectively. Quantitative RT-PCR showed that the mgTLR5 gene of the goose is widely expressed in all tested tissues, with the highest expression in the kidney and spleen. The increase in NF-κB promoter activity stimulated by flagellin was dependent on mgTLR5 expression in 293 T cells. Salmonella pullorum and flagellin significantly upregulated the expression of TLR5, IL-8, and IL-1 mRNA in peripheral blood mononucleotide cells of Magang goose cultured in vitro. Stimulation by S. pullorum for 24 h upregulated mgTLR5 expression in the cecum and kidney. We conclude that Magang goose TLR5 is a functional TLR5 homologue of the protein in other species and plays an important role in bacterial recognition.