Immunomodulation of helicobacter infection

Abstract

Helicobacter pylori leads to a chronic infection in humans that is associated with gastric inflammation and a vigorous immune response. Despite the humoral and cellular responses that can be detected in both human and animal models of helicobacter infection, the immune response fails to eliminate the organism. Eradication failure may be due to the niche in which H pylori confines itself, well away from direct contact with elements of the immune system. Alternatively, the general tendency of the intestinal immune response to down-regulate reactivity to noninvasive luminal bacteria also may contribute to the failure to eliminate helicobacter infection. Results of vaccine studies in mouse models indicate that modulating the helper T cell response from a T helper cell type 1 to a T helper cell type 2 response likely is required for the prevention and elimination of helicobacter infection. Understanding the mechanisms by which the immune response controls bacterial infections will allow for the design of novel strategies of immune modulation and the development of vaccines for both the treatment and prevention of H pylori.