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B in Gastric Epithelial Cells1
,
*
Division of Infectious Diseases, Department of Medicine,
Department of Microbiology and Immunology, and
Department of Cell Biology, Vanderbilt University School of Medicine, Nashville, TN 37232
In vivo, gastric infection with Helicobacter pylori
leads to substantial production of the inflammatory cytokines IL-1,
IL-6, TNF-
, and IL-8. H. pylori strains that contain the
cag pathogenicity island
(cag+) and are associated with
ulceration and gastric carcinoma induce greater cytokine production
than cag- strains. Expression of these
cytokines is often regulated by the transcription factor complex,
nuclear factor-
B (NF-B) through B-binding elements in the
enhancer/promoter regions of their genes. We report that more virulent
cag+ H. pylori strains induce
increased NF-B-DNA binding activity, which elevates IL-8 expression
in AGS gastric epithelial cells. The cag+
H. pylori strains induce significant stimulation of IL-8
promoter-driven reporter activity, while cag-
strains do not. Furthermore, mutation of specific genes within the
cag island (picA1 and picB)
ablates enhanced NF-B activation and IL-8 transcription. Increased
IL-8 expression is inhibited by mutation in either the NF-B or
NF-IL-6 binding element. The cag+ strains,
compared with the cag- strains, induce
enhanced nuclear localization of a RelA-containing NF-B binding
complex, but no increase in NF-IL-6 binding activity. These studies
demonstrate that the ability of different types of H.
pylori strains to activate NF-B correlates with their ability
to induce IL-8 transcription and indicate a mechanism for the
heightened inflammatory response seen in subjects infected with
cag+ H. pylori strains.
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