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.

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The potential threat of global warming in the 21st 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.

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