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T4SS-dependent TLR5 activation by Helicobacter pylori infection.

  • Pachathundikandi SK Department of Biology, Division of Microbiology, Friedrich Alexander University Erlangen-Nuremberg, Erlangen, Germany.
  • Tegtmeyer N Department of Biology, Division of Microbiology, Friedrich Alexander University Erlangen-Nuremberg, Erlangen, Germany.
  • Arnold IC Institute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland.
  • Lind J Department of Biology, Division of Microbiology, Friedrich Alexander University Erlangen-Nuremberg, Erlangen, Germany.
  • Neddermann M Department of Biology, Division of Microbiology, Friedrich Alexander University Erlangen-Nuremberg, Erlangen, Germany.
  • Falkeis-Veits C Institute for Pathology, Klinikum Bayreuth, Bayreuth, Germany.
  • Chattopadhyay S JIS Institute of Advanced Studies and Research, JIS University, Kolkata, 700091, India.
  • Brönstrup M Department of Chemical Biology, Helmholtz Centre for Infection Research, Braunschweig, Germany.
  • Tegge W Department of Chemical Biology, Helmholtz Centre for Infection Research, Braunschweig, Germany.
  • Hong M Division of Biological Science and Technology, Yonsei University, Wonju, Republic of Korea.
  • Sticht H Institute of Biochemistry, Division of Bioinformatics, Friedrich Alexander University Erlangen-Nuremberg, Erlangen, Germany.
  • Vieth M Institute for Pathology, Klinikum Bayreuth, Bayreuth, Germany.
  • Müller A Institute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland.
  • Backert S Department of Biology, Division of Microbiology, Friedrich Alexander University Erlangen-Nuremberg, Erlangen, Germany. Steffen.Backert@fau.de.
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  • 2019-12-18
Published in:
  • Nature communications. - 2019
Animals
Bacterial Proteins
Biopsy
Disease Models, Animal
Female
Gastric Mucosa
Helicobacter Infections
Helicobacter pylori
Host-Pathogen Interactions
Humans
Mice
Mice, Knockout
NF-kappa B
Signal Transduction
Toll-Like Receptor 5
Type IV Secretion Systems
English 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.
Language
  • English
Open access status
gold
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Persistent URL
https://sonar.ch/global/documents/3667
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