Is the Sanctuary WhereHelicobacter pyloriAvoids Antibacterial Treatment Intracellular?

Abstract

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.

Role of urease in megasome formation and Helicobacter pylori survival in macrophages

“…Ultimately, infected macrophages undergo apoptosis and viable bacteria and liberated [15,16]. In view of these data, it has been suggested that Hp occupy a protected intra-cellular niche that favors bacterial persistence and contributes to treatment failure [4,8,17].…”

Phosphoinositide3-kinase regulates actin polymerization during delayed phagocytosis ofHelicobacter pylori

“…[3]). In vivo, the ability of Hp to survive inside epithelial cells and macrophages contributes to organism persistence and treatment failure [4,5]. We have shown previously that type I Hp evade phagocytic killing and actively modulate their entry into macrophages, whereas the less-virulent type II strains do not [6].…”

Sulforaphane inhibits extracellular, intracellular, and antibiotic-resistant strains ofHelicobacter pyloriand prevents benzo[a]pyrene-induced stomach tumors

“…But even by the most optimistic estimates, these treatments are not universally successful (26,28). This lack of efficacy appears to be due, at least in part, to the development of resistance of H. pylori strains to these antibiotics (29,30) and the persistence of organisms within gastric epithelial cells (31,32). Moreover, the widespread use of antibiotics to eradicate H. pylori infections in developing countries is both logistically and economically impractical.…”