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- Ryoki Kobayashi
- Department of Microbiology and Immunology, Nihon University School of Dentistry at Matsudo, Chiba, 271–8587, Japan
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- Yasuhiro Ogawa
- Department of Oral Surgery, Nihon University School of Dentistry at Matsudo, Chiba, 271–8587, Japan
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- Tomomi Hashizume-Takizawa
- Department of Microbiology and Immunology, Nihon University School of Dentistry at Matsudo, Chiba, 271–8587, Japan
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- Tomoko Kurita-Ochiai
- Department of Microbiology and Immunology, Nihon University School of Dentistry at Matsudo, Chiba, 271–8587, Japan
説明
<jats:title>ABSTRACT</jats:title><jats:p>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.</jats:p>
収録刊行物
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- Pathogens and Disease
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Pathogens and Disease 78 (3), 2020-04-01
Oxford University Press (OUP)