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.

The potential threat of global warming in the 21^st century is on the ecosystem through many aspects, including the negative impact of rising global temperature on the health of humans and animals, especially domestic animals. The damage caused by heat stress to animals has been more and more significant as the worldwide climate continues to rise, along with the breeding industry’s expanding scale and stocking density, and it has become the most important stress‐causing factor in southern China. In this review, we described the effects of heat stress on animal immune organs and immune system. The much‐debated topic is how hyperthermia affects the tight junction barrier. Heat stress also induces inflammation in the body of animals causing low body weight and loss of appetite. This review also discussed that heat stress leads to hepatic disorder, and it also damages the intestine. The small intestine experiences ischemia, and the permeability of the intestine increases. Furthermore, the oxidative stress and mitogen‐activated protein kinase (MAPK) pathways have a significant role in stress‐induced cellular and organ injury. The study has shown that MAPK activity in the small intestine was increased by heat stress. Heat stress caused extreme small intestine damage, enhanced oxidative stress, and activated MAPK signaling pathways.

Herein, we assessed the anti-inflammatory and intestinal barrier protective effects of butyrolactone-I (BTL-1), derived from the coral-derived endophytic fungus (Aspergillus terreus), using the LPS-induced IPEC-J2 inflammation model and the DSS-induced IBD model in mice. In IPEC-J2 cells, pretreatment with BTL-I significantly inhibited TLR4/NF-κB signaling pathway and JNK phosphorylation, resulting in the decrease of IL-1β and IL-6 expression. Interestingly, BTL-1 pretreatment activated the phosphorylation of ERK and P38, which significantly enhanced the expression of TNF-α. Meanwhile, BTL-1 pretreatment upregulated tight junction protein expression (ZO-1, occludin, and claudin-1) and maintained intestinal barrier and intestinal permeability integrity. In mice, BTL-1 significantly alleviated the intestinal inflammatory response induced by DSS, inhibited TLR4/NF-κB signaling pathway, and MAPK signaling pathway, thus reducing the production of IL-1, IL-6, and TNF-α. Further, the expression of tight junction proteins (ZO-1, occludin, and claudin-1) was upregulated in BTL-1 administrated mice. Therefore, it has been suggested that butyrolactone-I alleviates inflammatory responses in LPS-stimulated IPEC-J2 and DSS-induced murine colitis by TLR4/NF-κB and MAPK signal pathway. Thereby, BTL-1 might potentially be used as an ocean drug to prevent intestinal bowel disease.

Macrophomina phaseolina is a vital seed and soil-borne phytopathogen responsible for substantial crop yield losses. Although various methods exist for managing soil-borne pathogens, such as agronomic practices, chemical treatments, and varietal tolerance, biological control utilizing plant growth-promoting rhizobacteria (PGPR) or their secondary metabolites presents promising avenues. In this study, a screening of 150 isolates from the rhizosphere of Vigna radiata L. was conducted to identify strains capable of promoting host growth and controlling charcoal rot disease. Among the tested isolates, only 15 strains demonstrated the ability to produce plant growth-related metabolites, including indole acetic acid, hydrogen cyanide, ammonia, and lytic enzymes, and solubilize inorganic phosphate. Subsequently, these potent strains were evaluated for their antifungal activity against Macrophomina phaseolina in vitro. Three strains, namely MRP-7 (58% growth inhibition), MRP-12 (55% growth inhibition), and MRP-8 (44% growth inhibition), exhibited the highest percent growth inhibition (PGI.). Furthermore, a pot experiment demonstrated that the selected strains acted as effective growth promoters and ROS (reactive oxygen species) scavengers, and served as potential biocontrol agents, significantly reducing the incidence of charcoal rot disease and improving various agronomic attributes of the host plant. These findings highlight the potential of these strains to be utilized as biofertilizers and biocontrol agents for sustainable agricultural practices.

The mammary glands, responsible for milk secretion, are regulated at a local level by various hormones, growth factors, non-coding RNAs, and other elements. Recent research has discovered the presence of lncRNAs in these glands, with suggestions that they may be essential for the maintenance and function of mammary glands. Besides directly controlling the gene and protein expression, lncRNAs are believed to play a significant part in numerous physiological and pathological processes. This study focused on examining the mammary gland tissues of Chinese Holstein cows, to identify and categorize long non-coding RNAs (lncRNAs). The research intended to distinguish lncRNAs in the mammary tissues of Holstein cows and contrast them between lactation and non-lactation periods. In this study, mammary gland tissues were sampled from three Holstein cows in early lactation (n = 3, 30 days postpartum) and non-lactation (n = 3, 315 days postpartum) on a large dairy farm in Jiangsu province. Mammary tissue samples were collected during early lactation and again during non-lactation. In total, we detected 1905 lncRNAs, with 57.3% being 500 bp and 612 intronic lncRNAs. The exon count for lncRNAs varied from 2 to 10. It was observed that 96 lncRNA expressions markedly differed between the two stages, with 83 genes being upregulated and 53 downregulated. Enrichment analysis results revealed that Gene Ontology (GO) analysis was primarily abundant in cellular processes. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis indicated that target genes were predominantly abundant in metabolic pathways, fatty acid biosynthesis, the immune system, and glycosphingolipid biosynthesis. This study analyzed the expression profile and characteristics of lncRNAs in the mammary gland tissues of Holstein cows during both lactation and non-lactation stages, forming a foundation for further investigation into the functional roles of lncRNAs in Holstein cows throughout lactation.