Immunomodulation of helicobacter infection

Helicobacter pylori leads to a chronic infection in humans that is associat ed with gastric inflammation and a vigorous immune response. Despite the hu moral and cellular responses that can be detected in both human and animal models of helicobacter infection, the immune response fails to eliminate th e organism. Eradication failure may be due to the niche in which H pylori c onfines itself, well away from direct contact with elements of the immune s ystem. Alternatively, the general tendency of the intestinal immune respons e to downregulate reactivity to noninvasive luminal bacteria also may contr ibute to the failure to eliminate helicobacter infection. Results of vaccin e studies in mouse models indicate that modulating the helper T cell respon se 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. Und erstanding the mechanisms by which the immune response controls bacterial i nfections will al low for the design of novel strategies of immune modulati on and the development of vaccines for both the treatment and prevention of H pylori.