16S rRNA sequencing of feces from DSS mice after Aggregatibacter actinomycetemcomitans gavage

Chronic intestinal inflammation of the gastrointestinal tract is a hallmark of inflammatory bowel disease (IBD), and it has been shown that in mouse models of colitis, salivary bacteria associated with periodontitis may exacerbate colitis. However, the precise pathogenic bacteria and how they contribute to intestinal inflammation are still unknown. Here, we revealed that Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans), the periodontitis-related pathogen, might enhance the inflammatory symptoms of DSS-induced colitis in mice, which invade through the gastrointestinal system. The colonization of A. actinomycetemcomitans in damaged intestinal tissues increased, but it had a constrained capacity for pathogenicity expansion. Additional research and analysis showed that the treatment of A. actinomycetemcomitans decreased the expression of tight junction protein ZO-1 and mucin MUC-2 in colitis mice, increased the expression of inflammatory factors, inspired the disorder of intestinal microbial barrier and the expansion of harmful pathogenic bacteria. In conclusion, A. actinomycetemcomitans triggered dysregulation of inflammatory factor expression and microbiota in colitis mice by affecting barrier integrity, implying that particular periodontal microbes should be targeted to decrease their impact on intestinal inflammation.