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The Effects of Oral Bacteria on Intestinal Flora and Immunity in Mice

• Oral microbiota have been linked to systemic diseases such as cardiovascular disease, bacterial pneumonia, diabetes mellitus, and low birth weight.

• Periodontal disease, caused by Porphyromonas gingivalis, is associated with atherosclerosis, diabetes, and low birth weight in infants.

• Streptococci, the most abundant bacteria in the oral cavity, are the causative agent of bacterial endocarditis and aspiration pneumonia, and have been noted as a risk factor for coronary artery disease and intracerebral hemorrhage.

• Oral bacteria and their metabolites, as well as inflammatory agents produced by the bacteria, may pass through microvessels from the invaded gingiva into the bloodstream, causing disease directly or indirectly.

• Oral administration of P. gingivalis to mice alters the intestinal flora and serum metabolome, leading to endotoxemia and subsequent inflammation of the liver and adipose tissue.

• Infection of mice on a high-fat diet with Aggregatibacter actinomycetemcomitans led to nonalcoholic fatty liver disease (NAFLD) by altering the gut microbiota and glucose metabolism.

• This study compared the effects of oral Streptococci (S. mitis and S. salivarius) with those of periodontal pathogens (P. gingivalis and P. nigrescens) on the intestinal flora, metabolic byproducts, and intestinal immunity in mice.

• Mice were challenged orally with 0.1 mL of 5% carboxymethyl cellulose or 109 CFU/mouse of S. mitis, S. salivarius, P. gingivalis, or P. nigrescens, five times per week for 2 weeks.

• The most abundant genera in the sample administered CMC were Lactobacillus, Turicibacter, Clostridium, Bacteroides, and Staphylococcus.

• S. mitis and S. salivarius altered the composition of fecal microbiota, increasing the abundance of Turicibacter and Bacteroides, respectively.

• P. gingivalis and P. nigrescens reduced the abundance of Lactobacillus and increased the abundance of Mucispirillum.

• S. mitis and S. salivarius increased the frequency of Th17 cells in the lamina propria of the small intestine, while P. gingivalis and P. nigrescens decreased the frequency of Th17 cells and increased the frequency of Treg cells.Oral Bacteria Intake Induces Gut Dysbiosis and Reduces Intestinal Immunity in Mice

• Oral dysbiosis is associated with systemic and oral diseases

• Oral administration of Streptococcus and Porphyromonas gingivalis induces gut dysbiosis in mice

• Lactobacillus and Turicibacter decrease with the intake of oral bacteria, while Bacteroides, Staphylococcus, Clostridium, and Jeotgalicoccus increase

• Lactobacillus salivarius is the most abundant species in the control group and decreases with the inoculation of oral bacteria

• Th17 cell abundance and IgA production in the small intestine decrease with oral bacteria intake

• The M1/M2 macrophage ratio in the small intestine increases with oral bacteria intake

• Fecal IgA production decreases significantly with oral bacteria intake

• Oral administration of human oral bacteria may induce fluctuations in the murine intestinal microbiota and bacterial metabolites

• The inoculation of mice with human oral microbes is completely different from that of humans

• Dysbiosis of the gut microbiome may shape Treg/Th17 activities, influencing susceptibility to inflammatory diseases

• Lactobacillus may be important for maintaining intestinal homeostasis and may be useful as a positive control

• Dysbiosis of the intestinal bacterial microbiota due to oral bacteria intake, and related variations in organic acid levels, may lead to an inflammatory state.

Test your knowledge on the effects of oral bacteria on intestinal flora and immunity in mice with this informative quiz. Learn about the link between oral microbiota and systemic diseases, the role of periodontal disease-causing bacteria, and the impact of various oral bacteria on the intestinal microbiota and immune response in mice. Challenge yourself to understand the complex interactions between oral bacteria and the gut microbiome, and how dysbiosis may lead to inflammatory states and disease susceptibility. Don't miss the chance to expand your