Zinc Deficiency Reduces Intestinal Secretory Immunoglobulin A and Induces Inflammatory Responses via the Gut-Liver Axis.

Nutritional zinc (Zn) deficiency could impair immune function and affect bowel conditions. However, the mechanism by which Zn deficiency affects the immune function of gut-associated lymphoid tissue (GALT) remains unclear. We investigated how Zn deficiency affects the function of GALT and level of secretory IgA (sIgA), a key component of the intestinal immune barrier, its underlying mechanisms, and whether Zn deficiency induces bacterial translocation to the liver. As previous research has indicated that interleukin (IL)-4 administration or Zn supplementation has a beneficial effect on the spleen of Zn-deficient rats, we investigated whether these supplements reverse the GALT immune system. Five-week-old male rats were fed a standard diet, Zn-deficient diet supplemented with saline or IL-4 for 6 weeks, or Zn-deficient diet followed by a standard diet for 4 weeks. Zn deficiency suppressed sIgA secretion in the intestinal tract by affecting GALT function and induced inflammatory responses through bacterial translocation to the liver via the portal vein. Furthermore, IL-4 administration and Zn supplementation in rats with Zn deficiency elicited comparable beneficial effects on GALT function, suggesting that the administration of either IL-4 or Zn could prevent inflammatory response via bacterial translocation to the liver.