Abstract
Streptococcus mutans, a pathogen of dental caries, occasionally causes infective endocarditis following bacteremia. In our previous study, we found that S. mutans strains isolated from the blood of patients with bacteremia aggravated cerebral hemorrhage in stroke model mice, while we also incidentally observed abnormal intestinal conditions in those animals. Ulcerative colitis and Crohn's disease are types of chronic inflammatory bowel disease (IBD) characterized by repeated periods of remission and relapse. Although intestinal bacterial flora is known to be a potential risk factor for IBD, others remain unclear. In the present study, we investigated possible mechanisms of aggravation of IBD by S. mutans. Significant aggravation of colon inflammation and increased mortality were observed in mice administered with a specific S. mutans strain via the jugular vein, and administration of the neutralizing antibody against IFN-γ improved those conditions. As for the mechanism, we speculated that bacteria in the bloodstream survive for a longer duration by resisting clearance, which would be advantageous for later localization in liver tissue. Furthermore, bacteria possessing a cell-surface collagen-binding protein may demonstrate improved binding to hepatocytes. Subsequently, the infecting bacteria induce cytokines such as those related to IFN-γ secretion, leading to an imbalance in the immune system. Finally, our results indicated that bacteremia caused by various oral streptococcal species such as Streptococcus sanguinis may also be a risk factor for aggravation of colitis.
