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- Title
Helicobacter pylori initiates successful gastric colonization by utilizing L-lactate to promote complement resistance.
- Authors
Hu, Shuai; Ottemann, Karen M.
- 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. The complement system is a key protective response against infectious pathogens. Here, the authors show that Helicobacter pylori uses host L-lactate to generate a complement resistant state that promotes gastric colonisation.
- Subjects
HELICOBACTER pylori; GASTRIC mucosa; BLOODBORNE infections; HELICOBACTER pylori infections; COMPLEMENT activation; COLONIZATION (Ecology); GASTROINTESTINAL system
- Publication
Nature Communications, 2023, Vol 14, Issue 1, p1
- ISSN
2041-1723
- Publication type
Article
- DOI
10.1038/s41467-023-37160-1