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Why Should We Consider Potential Roles of Oral Bacteria in the Pathogenesis of Sjögren Syndrome?

최영림|조미라|Park Sung-Hwan|Chang Sung-Ho
대한면역학회 (The Korean Association of Immunologists)|2022.08|Immune Network|제22권 제4호|pp. 1-20|DOI 10.4110/in.2022.22.e32

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OralBacteriaDysbiosisPathogenesisSalivary glandSjogren syndrome

초록

Sjögren syndrome (SS) is a chronic autoimmune disorder that primarily targets the salivary and lacrimal glands. The pathology of these exocrine glands is characterized by periductal focal lymphocytic infiltrates, and both T cell-mediated tissue injury and autoantibodies that interfere with the secretion process underlie glandular hypofunction. In addition to these adaptive mechanisms, multiple innate immune pathways are dysregulated, particularly in the salivary gland epithelium. Our understanding of the pathogenetic mechanisms of SS has substantially improved during the past decade. In contrast to viral infection, bacterial infection has never been considered in the pathogenesis of SS. In this review, oral dysbiosis associated with SS and evidence for bacterial infection of the salivary glands in SS were reviewed. In addition, the potential contributions of bacterial infection to innate activation of ductal epithelial cells, plasmacytoid dendritic cells, and B cells and to the breach of tolerance via bystander activation of autoreactive T cells and molecular mimicry were discussed. The added roles of bacteria may extend our understanding of the pathogenetic mechanisms and therapeutic approaches for this autoimmune exocrinopathy.

Abstract

Sjögren syndrome (SS) is a chronic autoimmune disorder that primarily targets the salivary and lacrimal glands. The pathology of these exocrine glands is characterized by periductal focal lymphocytic infiltrates, and both T cell-mediated tissue injury and autoantibodies that interfere with the secretion process underlie glandular hypofunction. In addition to these adaptive mechanisms, multiple innate immune pathways are dysregulated, particularly in the salivary gland epithelium. Our understanding of the pathogenetic mechanisms of SS has substantially improved during the past decade. In contrast to viral infection, bacterial infection has never been considered in the pathogenesis of SS. In this review, oral dysbiosis associated with SS and evidence for bacterial infection of the salivary glands in SS were reviewed. In addition, the potential contributions of bacterial infection to innate activation of ductal epithelial cells, plasmacytoid dendritic cells, and B cells and to the breach of tolerance via bystander activation of autoreactive T cells and molecular mimicry were discussed. The added roles of bacteria may extend our understanding of the pathogenetic mechanisms and therapeutic approaches for this autoimmune exocrinopathy.

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Two Sjogren syndrome-associated oral bacteria, Prevotella melaninogenica and Rothia mucilaginosa, induce the upregulation of major histocompatibility complex class I and hypoxia-associated cell death, respectively, in human salivary gland cells이재원, 전수민, 최영님대한구강생물학회 · International Journal of Oral Biology2021 · 제46권 제4호Induction of Anti-Aquaporin 5 Autoantibody Production by Immunization with a Peptide Derived from the Aquaporin of Prevotella melaninogenica Leads to Reduced Salivary Flow in Mice권성훈, 김홍희, 노진성, 유덕균, 이아름, 이용희, 전수민, 정수한, 정준호, 주소연, 황시원, YoungnimChoi대한면역학회 · Immune Network2021 · 제21권 제5호Aged Sanroque Mice Spontaneously Develop Sjögren's Syndrome-like Disease박성환, 오연경, 윤지희, 장기석, 장은경, 조미라, 최석산대한면역학회 · Immune Network2019 · 제19권 제1호Type I Interferon Increases Inflammasomes Associated Pyroptosis in the Salivary Glands of Patients with Primary Sjögren's Syndrome곽승기, 박성환, 이재선, 이주하, 조미라, Se Gwang Jang, Seung-Min Hong대한면역학회 · Immune Network2020 · 제20권 제5호Induction of anti-aquaporin 5 autoantibodies by molecular mimicry in mice이아름, 최영님대한구강생물학회 · International Journal of Oral Biology2020 · 제45권 제4호Autoantibody-Mediated Dysfunction of Salivary Glands Leads to Xerostomia in SKG Mice윤지희, 장기석, 장은경, 정승준, 최석산, 황경균대한면역학회 · Immune Network2019 · 제19권 제6호

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