

Helicobacter pylori evasion of immune system detection:
            While the body does amount a vigorous local immune response to H. pylori, the bacteria can still survive well in the gastric region.   Studies have demonstrated that H. pylori inhibit antigen presentation and induce T cell apoptosis.   Recent studies have demonstrated that H. pylori’s VacA can stop the cell cycle in T cells and thus block the cellular immune response by blocking T cell proliferation. By blocking T cell proliferation and interfering with the cellular immune system signaling pathway, H. pylori VacA acts an immunosuppressive agent that allows the bacteria to survive in the host. Additionally, some strains of the H. pylori LPS can evade the innate immune system by evading surfactant protein D binding.

Not all the mechanisms of H. pylori’s evasion of the immune system are not known for certain as many treatments that have been able to eliminate the bacteria in vitro, have proven to be ineffective in vivo. One possible mechanism of H. pylori’s ability to evade the immune system relates to the inability of monocytes and macrophages to kill the bacteria.  Specifically, it is hypothesized that H. pylori’s low endotoxin potency could minimize phagocyte activation. Additionally, H. pylori can weaken the respiratory burst by induced synthesis of superoxidedismutase and catalase which are able to detoxify oxygen free radicals of the immune system response.  Recent data shows that H. pylori can resist phagocytosis by disrupting phagosome maturation by forming megasomes that contain multiple viable organisms.  Studies have shown that H. pylori can survive in macrophage phagosomes for up to 24 hours.  H. pylori can survive in these macrophage phagosomes because they are able to inhibit the fusion of phagosome with lysosomes.  Additionally, studies have shown that H. pylori strains that contain the cag pathogenicity island (cag PAI) are more capable of inhibiting their own phagocytic uptake.

H. pylori bacteria also the unique ability of evading the immune response even after detection.  For example, studies in mice have shown that while anti-H. pylori IgA can recognize the bacteria, the rate of bacterial infection has no change between IgA deficient mice and mice containing IgA.  Even more interesting is the role of IL10 in H. pylori infection.  Studies have shown that IL-10 deficient mice have a significantly lower infection than mice that contain IL-10. 

            In addition to having to fight the host immune system, H. pylori survival is also threatened by the gastritis that it causes in the stomach.  Studies show that the gastritis caused by H. pylori cause ulcers which hurt both the host and H. pylori’s ability to survive.  However, recent studies have shown that H. pylori protect themselves from gastritis by internalizing themselves in the vacuoles of gastric epithelial cells. 

IgA Antibodies Impair Resistance against Helicobacter pylori Infection: Studies on Immune Evasion in IL-10-Deficient MiceAli A. Akhiani, Anneli Stensson, Karin Schon, and Nils Y. Lycke

Helicobacter Pylori Infection, Immune Response and Vaccination.  A. Lembo, L. Caradonna, T. Magrone, M. L. Mastronardi, D. Caccavo, E. Jirillo, L. Amati.

Immunobiology: The Immune System in Health and Disease 6th ed.  Charles A. Janeway Jr. et al.  2005.

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