Inflammatory bowel disease (IBD) is becoming an increasingly serious health problem in humans and animals. Probiotics can inhibit the development of IBD. Due to the specificity of the strains, the function and mechanism of action of different strains are still unclear. Here, a DSS-induced colitis mouse model was utilized to investigate the ability and mechanism by which Lacticaseibacillus casei IB1 alleviates colitis. Treatment with L. casei IB1 improved DSS-induced colitis in mice, as indicated by increased body weight, colon length, and goblet cell numbers and decreased disease activity index (DAI), proinflammatory factor (TNF-α, IL-1β, and IL-6) levels, and histopathological scores after intake of IB1. IB1 supplementation also improved the expression of tight junction proteins and inhibited the activation of the MAPK and NF-κB signaling pathways to alleviate intestinal inflammation. In addition, IB1 rebalanced the intestinal microbial composition of colitis mice by increasing the abundance of Faecalibaculum and Alistipes and decreasing the abundance of Bacteroides and Escherichia_Shigella. In summary, L. casei IB1 showed great potential for relieving colitis by regulating the microbiota and restoring the epithelial barrier. It can be used as a potential probiotic for the prevention and treatment of UC in the future.

Although numerous studies have shown that the hypothalamic–pituitary–adrenal axis plays a vital role in the response to environmental stress by mediating the production of a series of hormones, the mechanism underlying these effects has not been elucidated. This study used proteomics techniques to investigate the differentially expressed proteins (DEPs) in the pituitary glands of pigs and to elucidate the potential changes in the immune–neuroendocrine system under heat stress (HS). In total, 2517 peptides corresponding to 205 proteins were detected. A comparison of the expression patterns between HSs and healthy controls revealed 56 DEPs, of which 31 were upregulated and 25 were downregulated. Ingenuity pathway analysis (IPA) was used to reveal the subcellular characteristics, functional pathways, regulatory networks, and upstream regulators of the identified proteins. The results showed that these differentially expressed proteins were involved in intercellular communication, interactions, apoptosis, nervous system development, functions, abnormalities and other functions, and in the regulatory network. Moreover, the upstream regulators of the differentially expressed proteins were mainly transcriptional regulators, hormones, and cytokines. Thus, the functional network and pathway analyses could provide insights into the complexity and dynamics of HS–host interactions and may accelerate our understanding of the mechanisms underlying HS.

Exposure to vomitoxin (DON) can negatively impact the intestinal health of livestock and poultry, leading to compromised nutrient absorption and utilization, resulting in slowed growth and reduced production efficiency. In this study, we synthesized carbonated chitosan montmorillonite intercalation complexes (CCM) through solution precipitation. The successful formation of intercalation complexes was confirmed by examining functional groups and surface features using infrared spectroscopy and scanning electron microscopy. To assess the impact of CCM on DON-infected mice, we established an experimental mouse model of jejunal inflammation induced by DON infection. We analyzed the effects of CCM on blood biochemical and conventional indices, jejunal inflammatory factors, pathological changes, and the expression of proteins in the MAPK pathways in DON-infected mice. Our results indicate that CCM effectively mitigates the adverse effects of DON on growth performance, jejunal injury, and the inflammatory response in mice. CCM supplementation alleviated the negative effects of DON infection on growth performance and reduced intestinal inflammation in mice. Moreover, CCM supplementation successfully inhibited the activation of the mitogen-activated protein kinase (MAPK) signaling pathway induced by DON. These findings suggest that the mitigating effect of CCM on DON-induced inflammatory injury in the murine jejunum is closely linked to the regulation of the MAPK signaling pathway.