Abstract
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.
Highlights
Heat stress (HS) can cause immunosuppression, intestinal barrier damage, and inflammation in animals that affect the digestion and absorption of nutrients and reduce feed reward [1, 2], and increase the sensitivity of animals to a variety of infectious diseases [3]
We found that the abundance of Turicibacter sangunis was negatively correlated with short chain fatty acids (SCFAs) metabolism, whereas the changes in the abundance of Megasphaera cf was positively correlated with SCFAs metabolism
When animals are exposed to high temperature environment, water loss by evaporation and heat dissipation of the body through the epidermis is increased, which may lead to electrolyte imbalance [38,39,40]
Summary
Heat stress (HS) can cause immunosuppression, intestinal barrier damage, and inflammation in animals that affect the digestion and absorption of nutrients and reduce feed reward [1, 2], and increase the sensitivity of animals to a variety of infectious diseases [3]. IBD is an inflammatory reaction caused by an imbalance between the immune system and intestinal microecosystem, induced by environmental factors on the basis of susceptible genes [8]. Cui et al found that HS can induce oxidative stress reaction, immune response, and apoptosis of liver cells in pigs, resulting in the damage of liver function [13, 14]. Oxidative stress caused by HS has been shown to damage mitochondria, cell membrane and protein, and affect the liver lipid metabolism and animal production performance [9]. HS affects the glomerular filtration and urine concentration function of the kidneys by inducing changes in the levels of body electrolytes, especially the balance of sodium, potassium, calcium, and chloride ions, and creatinine metabolism [15, 16]
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