Related Experiment Video
Updated: Oct 6, 2025

Assessment of Gut Barrier Integrity in Mice Using Fluorescein-Isothiocyanate-Labeled Dextran
Published on: November 18, 2022
Heat stress-induced mucosal barrier dysfunction is potentially associated with gut microbiota dysbiosis in pigs
Bing Xia1, Weida Wu2, Wei Fang1,3
1State Key Laboratory of Animal Nutrition, Institute of Animal Sciences, Chinese Academy of Agricultural Sciences, Beijing, 100193, China.
Abstract:
Heat stress (HS) can be detrimental to the gut health of swine. Many negative outcomes induced by HS are increasingly recognized as including modulation of intestinal microbiota. In turn, the intestinal microbiota is a unique ecosystem playing a critical role in mediating the host stress response. Therefore, we aimed to characterize gut microbiota of pigs' exposure to short-term HS, to explore a possible link between the intestinal microbiota and HS-related changes, including serum cytokines, oxidation status, and intestinal epithelial barrier function. Our findings showed that HS led to intestinal morphological and integrity changes (villus height, serum diamine oxidase [DAO], serum D-lactate and the relative expressions of tight junction proteins), reduction of serum cytokines (interleukin [IL]-8, IL-12, interferon-gamma [IFN-γ]), and antioxidant activity (higher glutathione [GSH] and malondialdehyde [MDA] content, and lower superoxide dismutase [SOD]). Also, 16S rRNA sequencing analysis revealed that although there was no difference in microbial α-diversity, some HS-associated composition differences were revealed in the ileum and cecum, which partly led to an imbalance in the production of short-chain fatty acids including propionate acid and valerate acid. Relevance networks revealed that HS-derived changes in bacterial genera and microbial metabolites, such as Chlamydia, Lactobacillus, Succinivibrio, Bifidobacterium, Lachnoclostridium, and propionic acid, were correlated with oxidative stress, intestinal barrier dysfunction, and inflammation in pigs. Collectively, our observations suggest that intestinal damage induced by HS is probably partly related to the gut microbiota dysbiosis, though the underlying mechanism remains to be fully elucidated.
Related Concept Videos
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
Mucosal Barrier of the Stomach
Within parietal cells, carbonic acid is first formed through the reaction of water and carbon dioxide. The dissociation of carbonic acid releases bicarbonate and hydrogen ions. The bicarbonate...
Peptic Ulcer Disease II: Pathophysiology
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
Pathophysiology of Peptic Ulcer Disease: Injurious Factors
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
What is Monogastric Digestion?
Physiology of Enteric Nervous System and Gut Health

