PURPOSE OF REVIEW: To highlight recent findings on pathogenic mechanisms and clinical associations which characterize the role of infectious agents as triggers for Sjögren's syndrome development. RECENT FINDINGS: Several candidate infectious agents have been identified to induce the autoimmune and inflammatory pathways leading to Sjögren's syndrome clinical appearance in the setting of a genetic background. This is reinforced by the demonstration that Sjögren's syndrome patients are characterized by higher prevalence of seropositivity to virus and bacterial agents in comparison with general population. Moreover, these agents may infect salivary gland epithelial cells. Stronger evidence confirmed the role of some viruses, like Epstein-Barr, as triggers of the disease and different mechanisms have been demonstrated to interplay. Recent experimental and clinical studies supported the adjunctive role of an altered buccal and intestinal microbial composition and chronic inflammatory response to Helicobacter pylori in disease induction. Finally, latent viral infections and immune system chronic stimulation induced by persistent infections may participate in disease lymphoproliferative evolution. SUMMARY: Different viral and bacterial agents have been identified as triggers in Sjögren's syndrome induction and contributors to the chronic immune system stimulation underlying lymphoproliferative complication. Deeper knowledge of involved microbial agents and pathogenic mechanisms linking Sjögren's syndrome and infections may help the identification of preventive therapeutic strategy.
PURPOSE OF REVIEW: To highlight recent findings on pathogenic mechanisms and clinical associations which characterize the role of infectious agents as triggers for Sjögren's syndrome development. RECENT FINDINGS: Several candidate infectious agents have been identified to induce the autoimmune and inflammatory pathways leading to Sjögren's syndrome clinical appearance in the setting of a genetic background. This is reinforced by the demonstration that Sjögren's syndrome patients are characterized by higher prevalence of seropositivity to virus and bacterial agents in comparison with general population. Moreover, these agents may infect salivary gland epithelial cells. Stronger evidence confirmed the role of some viruses, like Epstein-Barr, as triggers of the disease and different mechanisms have been demonstrated to interplay. Recent experimental and clinical studies supported the adjunctive role of an altered buccal and intestinal microbial composition and chronic inflammatory response to Helicobacter pylori in disease induction. Finally, latent viral infections and immune system chronic stimulation induced by persistent infections may participate in disease lymphoproliferative evolution. SUMMARY: Different viral and bacterial agents have been identified as triggers in Sjögren's syndrome induction and contributors to the chronic immune system stimulation underlying lymphoproliferative complication. Deeper knowledge of involved microbial agents and pathogenic mechanisms linking Sjögren's syndrome and infections may help the identification of preventive therapeutic strategy.