Affiliation:
1. Department of Microbiology and Immunology, Nihon University School of Dentistry at Matsudo, Chiba, 271–8587, Japan
2. Department of Oral Surgery, Nihon University School of Dentistry at Matsudo, Chiba, 271–8587, Japan
Abstract
ABSTRACT
Recently, it has been suggested that the oral administration of Porphyromonas gingivalis, a keystone pathogen for periodontal disease, induces dysbiosis of the mouse intestinal microbiota and affects intestinal barrier function. Since oral streptococci are the predominant oral bacterial group, we compared the effect of their oral administration on the intestinal tract compared to that of P. gingivalis. Swallowing oral bacteria caused gut dysbiosis, due to increased Bacteroides and Staphylococcus and decreased Lactobacillus spp. Furthermore, oral bacterial infection caused an increase in lactate and decreases in succinate and n-butyrate contents. In the small intestine, the decrease in Th17 cells was considered to be a result of oral bacterial infection, although the population of Treg cells remained unaffected. In addition, oral bacterial challenge increased the M1/M2 macrophage ratio and decreased the immunoglobulin A (IgA) antibody titer in feces. These results suggest that gut dysbiosis caused by oral bacteria may cause a decrease in Th17 cells and fecal IgA levels and an increase in the M1/M2 macrophage ratio, thereby promoting chronic inflammation.
Publisher
Oxford University Press (OUP)
Subject
Infectious Diseases,Microbiology (medical),General Immunology and Microbiology,General Medicine,Immunology and Allergy
Cited by
50 articles.
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