みなさま

歯周病の原因菌が侵害受容ニューロンを抑制する，という発見です．研究室にも来られたことのあるソウル国立大学歯学部のオ・セグ・ベー先生のチームの論文です．

Chung S, Kim D, Koh B, Ko YK, Lee K, Kim H, Kim HY, Yu M, Erdogan O, Staurengo-Ferrari L, Chiu IM, Davey ME, Choi Y, Oh SB. Direct cellular contact by Porphyromonas gingivalis suppresses nociceptor excitability and induces analgesia during inflammation. Sci Adv. 2026 Sep 25;12(39):eaee8088. doi: 10.1126/sciadv.aee8088. Epub 2026 Sep 25. PMID: 42789707; PMCID: PMC13614394.

Abstract

Pain often accompanies tissue injury and inflammation. However, in certain inflammatory contexts like periodontitis, nociceptive signaling is paradoxically suppressed. The mechanisms underlying this analgesic state remain poorly understood. Here, we investigated whether and how Porphyromonas gingivalis (Pg) interacts with sensory neurons to induce analgesia in models of inflammatory pain. Exposure to live Pg reversed inflammatory thermal and mechanical hypersensitivity without altering local inflammation or nerve innervation. This effect required direct physical contact mediated in part by an integrin α5-FimA interface and gingipain protease activity and was not reproduced by heat-killed bacteria, protease-deficient mutants, or Pg-derived extracellular vesicles. At the neuronal level, Pg contact induced membrane hyperpolarization, reduced excitability of sensory neurons, and suppressed release of the nociceptive neuropeptide calcitonin gene-related peptide (CGRP). Proteomic and functional analyses identified downregulation of Fxyd2, a regulatory subunit of the Na+/K+-ATPase, linking altered ionic homeostasis to nociceptor silencing. These findings define a contact-dependent mechanism that actively suppresses peripheral pain signaling during inflammation.