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- W4360989968 abstract "The complement system has long been appreciated for its role in bloodborne infections, but its activities in other places, including the gastrointestinal tract, remain elusive. Here, we report that complement restricts gastric infection by the pathogen Helicobacter pylori. This bacterium colonized complement-deficient mice to higher levels than wild-type counterparts, particularly in the gastric corpus region. H. pylori uses uptake of the host molecule L-lactate to create a complement-resistant state that relies on blocking the deposition of the active complement C4b component on H. pylori's surface. H. pylori mutants unable to achieve this complement-resistant state have a significant mouse colonization defect that is largely corrected by mutational removal of complement. This work highlights a previously unknown role for complement in the stomach, and has revealed an unrecognized mechanism for microbial-derived complement resistance." @default.
- W4360989968 created "2023-03-30" @default.
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- W4360989968 date "2023-03-27" @default.
- W4360989968 modified "2023-09-30" @default.
- W4360989968 title "Helicobacter pylori initiates successful gastric colonization by utilizing L-lactate to promote complement resistance" @default.
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- W4360989968 doi "https://doi.org/10.1038/s41467-023-37160-1" @default.
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