Interplay of the Gastric Pathogen Helicobacter pylori with Toll-Like Receptors.

Toll-like receptors (TLRs) are crucial for pathogen recognition and downstream signaling to induce effective immunity. The gastric pathogen Helicobacter pylori is a paradigm of persistent bacterial infections and chronic inflammation in humans. The chronicity of inflammation during H. pylori infecti...

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Publicado en:BioMed Research International Vol. 2015; pp. 1 - 13
Autores principales: Pachathundikandi, Suneesh Kumar, Lind, Judith, Tegtmeyer, Nicole, El-Omar, Emad M., Backert, Steffen
Formato: review tables/charts Journal Article
Publicado: Wiley-Blackwell 4/6/2015
Acceso en línea:Ver este registro en EBSCOhost
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      dt: 4/6/2015
      vid: 2015
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      pub: Wiley-Blackwell
      place: Malden, Massachusetts
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        10.1155/2015/192420
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        atl: Interplay of the Gastric Pathogen Helicobacter pylori with Toll-Like Receptors.
      aug:
        au:
          Pachathundikandi, Suneesh Kumar
          Lind, Judith
          Tegtmeyer, Nicole
          El-Omar, Emad M.
          Backert, Steffen
        affil: Department of Biology, Division of Microbiology, Friedrich Alexander University Erlangen-Nuremberg, Staudtstraße 5, 91058 Erlangen, Germany
      sug:
        subj:
          Helicobacter Pylori
          Helicobacter Infections Diagnosis
          Proteins Physiology
          Toll-Like Receptors
          Immunity
          Intracellular Signaling Peptides and Proteins
          Helicobacter Infections Physiopathology
          Receptors, Cell Surface
          Genes
      ab: Toll-like receptors (TLRs) are crucial for pathogen recognition and downstream signaling to induce effective immunity. The gastric pathogen Helicobacter pylori is a paradigm of persistent bacterial infections and chronic inflammation in humans. The chronicity of inflammation during H. pylori infection is related to the manipulation of regulatory cytokines. In general, the early detection of H. pylori by TLRs and other pattern recognition receptors (PRRs) is believed to induce a regulatory cytokine or chemokine profile that eventually blocks the resolution of inflammation. H. pylori factors such as LPS, HSP-60, NapA, DNA, and RNA are reported in various studies to be recognized by specific TLRs. However, H. pylori flagellin evades the recognition of TLR5 by possessing a conserved N-terminal motif. Activation of TLRs and resulting signal transduction events lead to the production of pro- and anti-inflammatory mediators through activation of NF-κB, MAP kinases, and IRF signaling pathways. The genetic polymorphisms of these important PRRs are also implicated in the varied outcome and disease progression. Hence, the interplay of TLRs and bacterial factors highlight the complexity of innate immune recognition and immune evasion as well as regulated processes in the progression of associated pathologies. Here we will review this important aspect of H. pylori infection.
      pubtype: Academic Journal
      doctype:
        review
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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