Role of Zinc in the Pathogenesis of Inflammatory Bowel Disease: From Trace Elements to Zinc Signaling

The pathogenesis of inflammatory bowel disease (IBD) involves a complex interaction of factors, including impaired intestinal barrier function, gut microbiome dysbiosis, abnormal immune and inflammatory responses, and genetic predispositions. Decreased serum zinc concentrations have been reported in patients with IBD. Zinc, an essential trace element, supports various enzymatic processes, and its deficiency has been shown to worsen intestinal inflammation and negatively impact clinical outcomes in IBD. Moreover, with the discovery of zinc transporters, it has become evident that intracellular zinc acts as a signaling molecule affecting cellular functions, particularly in the gastrointestinal tract. In this review, we explore the role of zinc in IBD pathogenesis, drawing on both clinical data and basic research, emphasizing the effects of zinc on inflammatory responses, especially cytokine production in macrophages.