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doi: 10.1242/10.1242/jcs.00518
Research Article |
1 Physiological Laboratory, University of Liverpool, Liverpool L69 3BX, UK
2 Department of Medicine, University of Liverpool, Liverpool L69 3BX, UK
3 Department of Medical Microbiology, University of Liverpool, Liverpool L69
3BX, UK
4 Department of Pathology, University of Liverpool, Liverpool L69 3BX, UK
* Author for correspondence (e-mail: avarro{at}liverpool.ac.uk)
Accepted 26 March 2003
Epithelial cell responses to bacterial infection include induction of
matrix metalloproteinase 7 (MMP-7). Here, we identify increased MMP-7
expression in the gastric epithelium in response to the oncogenic bacterium
Helicobacter pylori, and report on the mechanisms and consequences
for gastric epithelial cell migration. In patients infected with H.
pylori, there was increased MMP-7 in gastric biopsies detected by western
blot. MMP-7 was localized to the advancing edge of migrating gastric
epithelial cell colonies, including lamellipodia. Rates of spreading of
gastric gland cells were higher in H. pylori-infected cultures
compared with control, and this was inhibited by antisense oligonucleotides to
MMP-7. Complementary data were obtained in a gastric cancer cell line (AGS
cells). In the latter, H. pylori induced expression of an
MMP-7-luciferase promoter/reporter vector through mechanisms that involved
activation of Rho and Rac. RhoA acted through activation of both NF-
B
and AP-1, whereas Rac activated NF-B but not AP-1. MMP-7 is commonly
upregulated in gastric cancer; since H. pylori is a recognized
gastric carcinogen, the data suggest a new mechanism by which the bacterium
might predispose towards gastric neoplasia.
Key words: MMP-7, Migration, Helicobacter pylori, Gastric epithelium, Matrix metalloproteinase
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