Interplay of the Gastric PathogenHelicobacter pyloriwith Toll-Like Receptors

Abstract

Toll-like receptors (TLRs) are crucial for pathogen recognition and downstream signaling to induce effective immunity. The gastric pathogenHelicobacter pyloriis a paradigm of persistent bacterial infections and chronic inflammation in humans. The chronicity of inflammation duringH. pyloriinfection is related to the manipulation of regulatory cytokines. In general, the early detection ofH. pyloriby 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. pylorifactors such as LPS, HSP-60, NapA, DNA, and RNA are reported in various studies to be recognized by specific TLRs. However,H. pyloriflagellin 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 ofH. pyloriinfection.