Journal of oral microbiology · 2026
Aggregatibacter actinomycetemcomitans exacerbates colitis and perturbs the gut microbiota in a murine model.
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Chen Xu, Zhu Xiaoming, Liu Yiran, Ma Lu, Li Lu, Dong Jitong, Li Zirui, Wang Tianyao, Zhang Juan, Xu Yan
Аннотация
BACKGROUND: Chronic intestinal inflammation is a hallmark of inflammatory bowel disease (IBD). Studies suggest that salivary bacteria associated with periodontitis may exacerbate colitis, but the specific contributory microbes and mechanisms remain unclear.
PATIENTS AND METHODS: We analyzed stool samples from 28 IBD patients and 21 controls. Bacterial DNA was extracted and quantified using qPCR targeting Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans). In a murine model, C57BL/6 mice received DSS followed by daily oral gavage with A. actinomycetemcomitans. Disease activity, histopathology and the gut microbiota were evaluated.
RESULTS: Oral administration of A. actinomycetemcomitans exacerbated inflammatory symptoms in DSS-induced colitis. The bacterium was detectable in intestinal tissue transiently following high-dose oral administration during the inflammatory phase. Following high-dose gavage, bacterial DNA was transiently detectable in intestinal tissue during inflammation. This treatment was associated with reduced expression of the tight junction protein ZO-1 and mucin MUC-2, elevated inflammatory mediators, and altered gut microbial community structure, including an expansion of taxa associated with dysbiosis.
CONCLUSION: In a murine colitis model, A. actinomycetemcomitans exposure was associated with worsened disease severity, coinciding with impaired barrier integrity, heightened inflammation and gut microbiota alterations. These exploratory findings highlight the potential role for specific periodontal microbes in modulating intestinal inflammation and warrant further investigation.
PATIENTS AND METHODS: We analyzed stool samples from 28 IBD patients and 21 controls. Bacterial DNA was extracted and quantified using qPCR targeting Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans). In a murine model, C57BL/6 mice received DSS followed by daily oral gavage with A. actinomycetemcomitans. Disease activity, histopathology and the gut microbiota were evaluated.
RESULTS: Oral administration of A. actinomycetemcomitans exacerbated inflammatory symptoms in DSS-induced colitis. The bacterium was detectable in intestinal tissue transiently following high-dose oral administration during the inflammatory phase. Following high-dose gavage, bacterial DNA was transiently detectable in intestinal tissue during inflammation. This treatment was associated with reduced expression of the tight junction protein ZO-1 and mucin MUC-2, elevated inflammatory mediators, and altered gut microbial community structure, including an expansion of taxa associated with dysbiosis.
CONCLUSION: In a murine colitis model, A. actinomycetemcomitans exposure was associated with worsened disease severity, coinciding with impaired barrier integrity, heightened inflammation and gut microbiota alterations. These exploratory findings highlight the potential role for specific periodontal microbes in modulating intestinal inflammation and warrant further investigation.