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T4SS-dependent TLR5 activation by Helicobacter pylori infection.
Pachathundikandi, Suneesh Kumar Tegtmeyer, Nicole Arnold, Isabelle Catherine Lind, Judith Neddermann, Matthias Falkeis-Veits, Christina Chattopadhyay, Sujay Hong, Minsun
Pachathundikandi, Suneesh Kumar
Tegtmeyer, Nicole
Arnold, Isabelle Catherine
Lind, Judith
Neddermann, Matthias
Falkeis-Veits, Christina
Chattopadhyay, Sujay
Hong, Minsun
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2019-12-16
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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+ 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.
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Nat Commun. 2019 Dec 16;10(1):5717. doi: 10.1038/s41467-019-13506-6.
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en
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2041-1723
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Attribution-NonCommercial-ShareAlike 4.0 International