AI Article Synopsis

  • Host cells recognize cytosolic double-stranded DNA and cyclic dinucleotides through the STING molecule, triggering an innate immune response that produces Type I interferons and proinflammatory cytokines.
  • The review explores how bacterial cyclic dinucleotides and the STING/TBK1/IRF3 pathway may contribute to the development and immune regulation of periodontal disease.
  • It also discusses potential activators and inhibitors of the STING pathway, highlighting their promise in treating periodontitis and suggesting insights for future research into immune therapies.

Article Abstract

Host cells can recognize cytosolic double-stranded DNAs and endogenous second messengers as cyclic dinucleotides-including c-di-GMP, c-di-AMP, and cGAMP-of invading microbes via the critical and essential innate immune signaling adaptor molecule known as STING. This recognition activates the innate immune system and leads to the production of Type I interferons and proinflammatory cytokines. In this review, we (1) focus on the possible role of bacterial cyclic dinucleotides and the STING/TBK1/IRF3 pathway in the pathogenesis of periodontal disease and the regulation of periodontal immune response, and (2) review and discuss activators and inhibitors of the STING pathway as immune response regulators and their potential utility in the treatment of periodontitis. PubMed/Medline, Scopus, and Web of Science were searched with the terms "STING", "TBK 1", "IRF3", and "cGAS"-alone, or together with "periodontitis". Current studies produced evidence for using STING-pathway-targeting molecules as part of anticancer therapy, and as vaccine adjuvants against microbial infections; however, the role of the STING/TBK1/IRF3 pathway in periodontal disease pathogenesis is still undiscovered. Understanding the stimulation of the innate immune response by cyclic dinucleotides opens a new approach to host modulation therapies in periodontology.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8226932PMC
http://dx.doi.org/10.3390/pathogens10060675DOI Listing

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