Regulation of mucosal immune homeostasis in the intestine [7, 71, 78, 108, 123, 133]. The dynamic change in competition in zinc acquisition between the host and pathogens is complicated. In addition to playing a role in enzymes and structural cofactors for the survival of all organisms, zinc also affects the activity of some transmembrane receptor proteins, including TLRs, which are responsible for the recognition of microbes or antigen molecules and the development and modulation of immune responses. Upon pathogen attack, some zinc-sequestering proteins are expressed and recruited to the infected site to chelate zinc ions and limit the growth and virulence of pathogenic bacteria, such as calprotectin, also known as the S100A8/S100A9 heterodimer, which is vital for strategic nutritional immunity. During the infectious process, the host also releases other S100 proteins, and then the binding of S100 proteins to cell surface receptors, such as TLR4, RAGE, and GPCRs, plays an important role in the regulation of inflammatory signal transduction. In turn, by regulating downstream signalling pathways, zinc can enhance the integrity of the intestinal mucosal barrier and reduce inflammation and diarrhoea caused by pathogenic infection.