T4SS-dependent TLR5 activation by Helicobacter pylori infection

Suneesh Kumar P, Tegtmeyer N, Arnold IC, Lind J, Neddermann M, Falkeis-Veits C, Chattopadhyay S, Brönstrup M, Tegge W, Hong M, Sticht H, Müller A, Backert S, Vieth M (2019)

Publication Type: Journal article

Publication year: 2019


Book Volume: 10

Article Number: 5717

Journal Issue: 1

DOI: 10.1038/s41467-019-13506-6


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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Suneesh Kumar, P., Tegtmeyer, N., Arnold, I.C., Lind, J., Neddermann, M., Falkeis-Veits, C.,... Vieth, M. (2019). T4SS-dependent TLR5 activation by Helicobacter pylori infection. Nature Communications, 10(1). https://doi.org/10.1038/s41467-019-13506-6


Suneesh Kumar, Pachathundikandi, et al. "T4SS-dependent TLR5 activation by Helicobacter pylori infection." Nature Communications 10.1 (2019).

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