Oral Vaccination Against Helicobacter pyloriInfection Is Not Effective in Mice With Fas Ligand Deficiency

The aim of this study was to delineate the role of the Fas pathway in vaccination against Helicobacter pylori. C57BL/6 and Fas ligand–deficient (gld) mice were divided into 3 groups: control, H. pyloriinfected, and orally vaccinated (H. pyloriwhole cell sonicate and cholera toxin adjuvant). Oral vaccination prevented H. pyloricolonization in 78% of C57BL/6 mice compared to only 18% of gldmice. Vaccination did not alter the degree of apoptosis in either strain of mice. Vaccination led to significant increase in interleukin (IL)-5 and IL-10 in C57BL/6 but not gldmice. H. pyloriinfection increased interferon (IFN)-γ levels in C57BL/6 but not in gldmice while vaccination had no effect on IFN-γ levels in either strain. Oral vaccination is not effective in Fas ligand–deficient mice likely owing to lack of effective cytokine responses. This indicates that the Fas pathway plays a critical role in promoting an appropriate effector response following H. pylorivaccination.

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