T4SS-dependent TLR5 activation by Helicobacter pylori infection.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 31844047.
- Also identified by DOI 10.1038/s41467-019-13506-6 and PMC identifier 6915727.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
Toll-like receptor TLR5 recognizes a conserved domain, termed D1, that is present in flagellins of several pathogenic bacteria but not in Helicobacter pylori. Highly virulent H. pylori strains possess a type IV secretion system (T4SS) for delivery of virulence factors into gastric epithelial cells. Here, we show that one of the H. pylori T4SS components, protein CagL, can act as a flagellin-independent TLR5 activator. CagL contains a D1-like motif that mediates adherence to TLR5<sup>+</sup> epithelial cells, TLR5 activation, and downstream signaling in vitro. TLR5 expression is associated with H. pylori infection and gastric lesions in human biopsies. Using Tlr5-knockout and wild-type mice, we show that TLR5 is important for efficient control of H. pylori infection. Our results indicate that CagL, by activating TLR5, may modulate immune responses to H. pylori.
Medical subject headings
- Bacterial Proteins
- Helicobacter Infections
- Helicobacter pylori
- Toll-Like Receptor 5
- Type IV Secretion Systems