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

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.

Requirements for anti‐aquaporin 5 autoantibody production in a mouse model

“…Indeed, only 11% of mice immunized with Pm lysate produced anti‐AQP5E autoantibodies in our previous study (Lee et al., 2021). Therefore, the prevalent production of high levels of anti‐AQP5 autoantibodies detected in patients with Sjogren's syndrome may be attributed to the chronic bacterial infection of the salivary glands, including Pm, and the genetic susceptibility of patients (Alam et al., 2020; Chang et al., 2022; Nocturne & Mariette, 2018).…”