Emerging evidence highlights the oral–gut axis as an important contributor to the pathogenesis of inflammatory bowel disease (IBD); however, the specific role of the tongue coating microbiota remains poorly understood. To comprehensively delineate oral–gut microbial alterations in IBD, we analyzed tongue coating and fecal microbiota from 596 participants, including 278 patients with Crohn’s disease (CD), 91 with ulcerative colitis (UC), and 227 healthy controls (HCs), using 16S ribosomal RNA (rRNA) gene sequencing. Patients with IBD exhibited a distinct dysbiotic signature in tongue coating microbiota, characterized by increased abundances of Streptococcus , Prevotella , and Gemella in both CD and UC patients, alongside a CD-specific depletion of commensal taxa such as Neisseria and Fusobacterium compared with HCs. Notably, a similar oral microbial shift was observed in a spontaneous enteritis mouse model, which demonstrated enrichment of oral Streptococcus and concordant increases in Prevotella across both oral and intestinal niches. To establish causality, tongue coating microbiota from CD patients were transplanted into antibiotic-pretreated mice, resulting in significantly exacerbated colitis relative to recipients of HC-derived microbiota. Mechanistically, Streptococcus strains isolated from CD patients promoted Th1 cell polarization in vitro and aggravated colitis in vivo , implicating these orally derived pathobionts in the amplification of intestinal inflammation. Together, these findings identify the tongue coating microbiota as a previously underappreciated mediator of gut inflammation in IBD, support its potential utility as a non-invasive biomarker for CD, and provide mechanistic evidence that oral microbial dysbiosis can actively drive intestinal immune pathology.
Wang et al. (Sun,) studied this question.