Host defense peptides (HDPs) are primary components of the innate immune system with diverse biological functions, such as antibacterial ability and immunomodulatory function. HDPs are produced and released by immune and epithelial cells against microbial invasion, which are widely distributed in humans, animals, plants, and microbes. Notably, there are great differences in endogenous HDP distribution and expression in humans and animals. Moreover, HDP expression could be regulated by exogenous substances, such as nutrients, and different physiological statuses in health and disease. In this review, we systematically assessed the regulation of expression and mechanism of endogenous HDPs from nutrition and disease perspectives, providing a basis to identify the specificity and regularity of HDP expression. Furthermore, the regulation mechanism of HDP expression was summarized systematically, and the differences in the regulation between nutrients and diseases were explored. From this review, we provide novel ideas targeted the immune regulation of HDPs for protecting host health in nutrition and practical and effective new ideas using the immune regulation theory for further research on protecting host health from pathogenic infection and excessive immunity diseases under the global challenge of the antibiotic-abuse-induced series of problems, including food security and microbial resistance.

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BACKGROUND Ulcerative colitis is a gastrointestinal disease closely related to intestinal epithelial barrier damage and intestinal microbiome imbalance; however, effective treatment methods are currently limited. Rehmannia glutinosa polysaccharide (RGP) is an important active ingredient with a wide range of pharmacological activities, although its protective effect on colitis remains to be explored. In the present study, we verified the in vitro anti‐inflammatory effect of RGP, and observed the ameliorating effect of RGP on dextran sulfate sodium‐induced colitis in mice. RESULTS The results showed that (i) RGP attenuates lipopolysaccharide‐induced overexpression of inflammatory factors in RAW264.7 cells; (ii) RGP improves the pathological damage caused by DSS, including weight loss, increased disease activity index and intestinal tissue ulcers; (iii) RGP improves tight junction proteins to protects the tightness of the intestinal epithelium; (iv) RGP inhibits the expression of inflammatory factors through the nuclear factor‐kappa B pathway, and improved the of intestinal tissues inflammation; and (v) RGP can maintain the species diversity of intestinal microbes, increase the content of short‐chain fatty acids and then restore the imbalance of intestinal microecology. CONCLUSION RGP can improve the intestinal microbiota to strengthen the intestinal epithelial barrier and protect against DSS‐induced colitis. © 2022 Society of Chemical Industry.