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Gastric Ulcers: H. pylori Infection Alters ZO1 Localization

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For many years the cause of gastric ulcers was always attributed to poor diet. Several years ago, scientists revealed that a common intestinal bacterium called Helicobacter pylori was actually the causative agent. These bacterial cells attach via adhesions to the cell surface of epithelial cells in the gastric mucosa. Through the secretion of various cytoxins they disrupt the intestinal epithelium causing gastritis and in some individuals gastric cancer. Research into how the H. pylori infects cells has shown that it alters the junctional adhesion complexes of the gastric epithelium of humans. As shown in the following diagram, ZO1 localizes to the surface of all of the cells showing a relatively consistent pattern (Figure 3.11). This localization is altered in infected cells with some of the protein not only disappearing from the cell surface junctions but also appearing within the cytoplasm. Some of the protein can also be seen in some of the nuclei. Based on the function of ZO1 as a NACo, the release of ZO1 proteins from tight junctions results in their movement as soluble proteins in the cytoplasm and from there into the nucleus where they can alter gene activity.


Figure 3.11. A diagrammatic representation of the Localization of ZO1 (green = ZO1; blue = nuclei) in normal (A) human gastric epithelial cells and those infected with H. pylori (B).

Introduction to the Human Cell

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