TY - JOUR
T1 - Oral bacteria affect the gut microbiome and intestinal immunity
AU - Kobayashi, Ryoki
AU - Ogawa, Yasuhiro
AU - Hashizume-Takizawa, Tomomi
AU - Kurita-Ochiai, Tomoko
N1 - Publisher Copyright:
© FEMS 2020. All rights reserved.
PY - 2020
Y1 - 2020
N2 - 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.
AB - 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.
KW - Gut dysbiosis
KW - IgA
KW - Inflammation
KW - M1/M2 macrophage ratio
KW - Oral bacteria
KW - Th17 cells
UR - http://www.scopus.com/inward/record.url?scp=85086522718&partnerID=8YFLogxK
U2 - 10.1093/FEMSPD/FTAA024
DO - 10.1093/FEMSPD/FTAA024
M3 - Article
C2 - 32504490
AN - SCOPUS:85086522718
SN - 2049-632X
VL - 78
JO - Pathogens and Disease
JF - Pathogens and Disease
IS - 3
M1 - ftaa024
ER -