| Popis: |
Initial responses to gastric colonization by Helicobacter pylori include a transient period of achlorhydria and activation of neutrophils (1). In our previous work (2) we showed that acute bacterial infection of human gastric adenocarcinoma cells (AGS) inhibits the activity of human H,K-ATPase α subunit promoter, which may contribute to lowered acid output found in acute H. pylori infection in vivo. The inflammatory response is hypothesized to be induced both directly by bacterial factors like LPS, urease, porins, etc and indirectly by induction of the chemokine IL-8 and cytokines (IL-1, TNFα), leading to mucosal damage and ulceration (1). Matrix metalloproteinases play major roles in tissue degradation, cell migration and also inflammatory processes. We have previously shown that H. pylori infection of AGS cells increased secretion of epithelial MMPs-1 and -3 and bacterial MMP-3-like activity (3). Our aim in the present study was to characterize the relationship between activation of matrix metalloproteinases and IL-1β and TNFα, potent stimulators of IL-8 secretion in gastric epithelia during H pylori infection. |
