<oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:creator>Pachathundikandi SK</dc:creator>
  <dc:creator>Tegtmeyer N</dc:creator>
  <dc:creator>Arnold IC</dc:creator>
  <dc:creator>Lind J</dc:creator>
  <dc:creator>Neddermann M</dc:creator>
  <dc:creator>Falkeis-Veits C</dc:creator>
  <dc:creator>Chattopadhyay S</dc:creator>
  <dc:creator>Brönstrup M</dc:creator>
  <dc:creator>Tegge W</dc:creator>
  <dc:creator>Hong M</dc:creator>
  <dc:creator>Sticht H</dc:creator>
  <dc:creator>Vieth M</dc:creator>
  <dc:creator>Müller A</dc:creator>
  <dc:creator>Backert S</dc:creator>
  <dc:date>2019</dc:date>
  <dc:description xmlns:ns0="xml" ns0:lang="en">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.</dc:description>
  <dc:format>application/pdf</dc:format>
  <dc:identifier>https://sonar.ch/global/documents/3667</dc:identifier>
  <dc:language>eng</dc:language>
  <dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.1038/s41467-019-13506-6</dc:relation>
  <dc:relation>info:eu-repo/semantics/altIdentifier/pmid/31844047</dc:relation>
  <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
  <dc:source>Nature communications. - 2019</dc:source>
  <dc:subject xmlns:ns1="xml" ns1:lang="en">Animals</dc:subject>
  <dc:subject xmlns:ns2="xml" ns2:lang="en">Bacterial Proteins</dc:subject>
  <dc:subject xmlns:ns3="xml" ns3:lang="en">Biopsy</dc:subject>
  <dc:subject xmlns:ns4="xml" ns4:lang="en">Disease Models, Animal</dc:subject>
  <dc:subject xmlns:ns5="xml" ns5:lang="en">Female</dc:subject>
  <dc:subject xmlns:ns6="xml" ns6:lang="en">Gastric Mucosa</dc:subject>
  <dc:subject xmlns:ns7="xml" ns7:lang="en">Helicobacter Infections</dc:subject>
  <dc:subject xmlns:ns8="xml" ns8:lang="en">Helicobacter pylori</dc:subject>
  <dc:subject xmlns:ns9="xml" ns9:lang="en">Host-Pathogen Interactions</dc:subject>
  <dc:subject xmlns:ns10="xml" ns10:lang="en">Humans</dc:subject>
  <dc:subject xmlns:ns11="xml" ns11:lang="en">Mice</dc:subject>
  <dc:subject xmlns:ns12="xml" ns12:lang="en">Mice, Knockout</dc:subject>
  <dc:subject xmlns:ns13="xml" ns13:lang="en">NF-kappa B</dc:subject>
  <dc:subject xmlns:ns14="xml" ns14:lang="en">Signal Transduction</dc:subject>
  <dc:subject xmlns:ns15="xml" ns15:lang="en">Toll-Like Receptor 5</dc:subject>
  <dc:subject xmlns:ns16="xml" ns16:lang="en">Type IV Secretion Systems</dc:subject>
  <dc:title xmlns:ns17="xml" ns17:lang="en">T4SS-dependent TLR5 activation by Helicobacter pylori infection.</dc:title>
  <dc:type>http://purl.org/coar/resource_type/c_6501</dc:type>
</oai_dc:dc>
