I s t h e S a n c t u a r y W h e r e Helicobacter pylori A v o i d s A n t i b a c t e r i a l T r e a t m e n t I n t r a c e l l u l a r ? This work was supported in part by grants 10617 and 10848 from the Swedish Medical Research Council, the Nanna Svartz Foundation (L.E.), the Department of Veterans Affairs, the support of Tom and Pat Powers Foundation, and Hilda Schwartz (D.G.).Manuscript received September 18, 1996; revision accepted February 19,1997. Address reprint requests to Dr Engstrand: Department of Clinical Microbiology, University Hospital, S-751 85, Uppsala, Sweden. and HLA-DR was always observed, indicating an ongoing local immune response. Infection was cleared on day 14, but when examined 4 weeks after completion of therapy, Genta staining indicated that only five volunteers remained free of H pylori. However, results of immunohistochemical staining were negative at this time for only two volunteers. Disappearance of intracellular expression of bacterial HSP60 remained after therapy and correlated with the intensity of chronic inflammatory cell infiltration. These data are consistent with the intracellular localization of H pylori having a role in inflammation and as a protective strategy against extracellular antibacterial activity.

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