Search

Simple Summary: This review highlights the various adverse effects of heat stress on the production and general well-being of the goat industry. Goats possess exceptional adaptability traits, allowing them to thrive well in diverse environments, particularly in harsh conditions such as tropical and semi-arid zones. This makes goats the ideal small ruminants for food security in an era of inevitable and continuous climate change. Despite the inherent ability of goats to withstand extreme weather conditions, their reproductivity and overall productivity are compromised in the event of heat stress. Therefore, gaining in-depth knowledge of the effects of heat stress and the various mitigating strategies to alleviate heat stress is a significant approach to ensuring food security. These efforts will serve as a benchmark for genetically engineering heat-tolerant goats suitable for the current climatic conditions to ensure optimal productivity in the future. Goats, versatile creatures selectively bred for various purposes, have become pivotal in shaping the socioeconomic landscape, particularly in rural and economically challenged areas. Their remarkable ability to withstand and adapt to extreme heat has proven invaluable, allowing them to flourish and reproduce in even the harshest climates on Earth. Goat farming has emerged as a reliable and sustainable solution for securing food resources. However, despite its significance, the goat-producing industry has received less attention than other ruminants. Despite goats' inherent resilience to heat, their productivity and reproductive performance suffer under high ambient temperatures, leading to heat stress. This presents a significant challenge for goat production, necessitating a comprehensive multidisciplinary approach to mitigating the adverse effects of heat stress. This review aims to explore the diverse impacts of heat stress on goats and propose effective measures to address the sector's challenges. By understanding and addressing these issues, we can enhance the resilience and sustainability of goat farming, ensuring its continued contribution to food security and socioeconomic development. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Heat stress is a widespread phenomenon in domestic animal feeding in tropical and sub-tropical areas that are subjected to a growing negative effect in livestock and poultry due to global warming. It leads to reduced food intake, retarded growth, intestinal disequilibrium, lower reproductive performance, immunity and endocrine disorders in livestock and poultry. Many studies show that the pathogenesis of heat stress is mainly related to oxidative stress, hormone secretion disorder, cytokine imbalance, cell apoptosis, cell autophagy, and abnormal cell function. Its mechanism refers to activation of mitogen-activated protein kinase (MAPK) signaling pathway and nuclear factor kappa B (NF-κB) signaling pathway, the fluctuation of tight junction protein and heat shock protein expression, and protein epigenetic modification. This manuscript reviews the mechanism of heat stress through an insight into the digestive, reproductive, immune, and endocrine system. Lastly, the progress in prevention and control techniques of heat stress has been summarized. • Heat stress damages animal digestive, reproductive, immune, and endocrine systems. • It results in decreased food intake, digestive, and reproductive performance. • It impairs intestinal barrier function and causes endocrine and immune disorders. [ABSTRACT FROM AUTHOR]

Heat stress (HS) has a negative impact on animal health. A modified chitosan-gentamicin conjugate (CS-GT) was prepared to investigate its potential protective effects and mechanism of action on heat stress-induced intestinal mucosa injury in IPEC-J2 cells and mouse 3D intestinal organs in a mouse model. CS-GT significantly (P < 0.01) reversed the decline in transmembrane resistance and increased the FITC-dextran permeability of the IPEC-J2 monolayer fusion epithelium caused by heat stress. Heat stress decreased the expression of the tight binding proteins occludin, claudin1, and claudin2. However, pretreatment with CS-GT significantly increased (P < 0.01) the expression of these tight binding proteins. Mechanistically, CS-GT inhibited the activation of the TLR4/STAT6/MYLK signaling pathway induced by heat stress. Molecular docking showed that CS-GT can bind effectively with TLR4. In conclusion, CS-GT alleviates heat stress-induced intestinal mucosal damage both in vitro and in vivo. This effect is mediated, at least partly, by the inhibition of the TLR4/STAT6/MYLK signaling pathway and upregulation of tight junction proteins. These findings suggest that CS-GT may have therapeutic potential in the prevention and treatment of heat stress-related intestinal injury. [Display omitted] [ABSTRACT FROM AUTHOR]

In many mammalian species, including pigs, heat stress (HS) detrimentally leads to epithelium damage and increases intestinal permeability. However, the underlying molecular mechanisms are not thoroughly investigated yet. This study aimed to examine the RIP1/RIP3-ERK1/2 signaling pathway that regulates the expression of tight junction proteins in HS-treated pigs. In in vitro cultured intestinal porcine epithelial cells (IPEC-J2), HS induced the expression of tight junction proteins, ZO-1, claudin-1, and claudin-4, that are regulated by the ERK1/2-MAPK signaling pathway. Further, high expression of HSP70 in IPEC-J2 cells induced a significant decrease in receptor-interacting protein 1/3 (RIP1/3), phosphorylated ERK, and tight junction protein claudin-1 (P < 0.05). Necrostatin-1 (A selective inhibitor of RIPK1) suppressed the upregulation of phosphorylated ERK1/2 induced by HS, indicating that the RIP1/RIP3 regulates ERK1/2 phosphorylation in IPEC-J2 under heat stress. In addition, HS significantly damaged the intestinal morphology characterized by reduction of villus length and crypt depth in in vivo porcine model. Moreover, the expression of tight junction, ZO-1, and claudin-4 were downregulated, whereas phosphorylated p38 and ERK1/2 were upregulated in the duodenum of heat-stressed pigs. Interestingly, a decrease in ZO-1 and claudin-1 was observed in the colon, where phosphorylated ERK1/2 was similar to that in the duodenum. Our results demonstrate that RIP1/RIP3-ERK1/2 signaling pathway regulates the expression of tight junction proteins in HS-pigs. This finding further advances the intestinal barrier function's underlying mechanisms associated with signaling regulation. • A heat stress induced porcine inflammatory bowel disease model was constructed successfully. • Heat stress induced down – regulation of tight junction proteins play a vital role in the development inflammatory bowel disease in pigs. • Heat stress induced down-regulation of tight junction proteins was via ERK1/2 signaling pathway. [ABSTRACT FROM AUTHOR]