ArticleFuture microbiology2013
Helicobacter pylori utilizes DNA shuffling to modulate the gastric inflammatory response.
Article in Future microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
Infections with the human gastric pathogen Helicobacter pylori are among the most common infections worldwide, causing a significant burden of disease due to their association with gastric carcinogenesis. A hallmark of acute and chronic H. pylori infection is intense inflammation in the gastric submucosa, which is strongly enhanced by the activity of a major bacterial virulence factor, the cytotoxin-associated gene (Cag)-type IV secretion system (T4SS). Despite intense research in recent years, the molecular mechanisms leading to proinflammatory signaling by the Cag-T4SS are only partly understood. Barrozo et al. now show that this proinflammatory capability of H. pylori can be reduced or increased in vivo by recombination events in a particular repeat region of the T4SS component CagY, and that lymphocytes are the main driving force triggering such events. The results highlight the mutual interplay between a major bacterial virulence factor and the immune system and might aid in understanding bacterial persistence.
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