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A Galleria mellonella Oral Administration Model to Study Commensal-Induced Innate Immune Responses
Published on: March 21, 2019
An orally administered oral pathobiont and commensal have comparable and innocuous systemic effects in germ-free mice
Keisuke Sato1,2, Mai Yokoji1,2, Miki Yamada1,2
1Research Unit for Oral-Systemic Connection, Division of Oral Science for Health Promotion, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Background And Objectives:
We recently proposed a novel mechanism linking periodontitis and systemic diseases, in which orally administered Porphyromonas gingivalis affects gut microbiota composition and subsequently leads to systemic inflammation. However, the mechanism by which P. gingivalis generates systemic effects from the gut is unknown.
Material And Methods:
Six-week-old germ-free mice were orally administered with either an oral pathobiont P. gingivalis or an oral commensal Lactobacillus salivarius twice a week for 5 weeks. Control mice were administered with vehicle only. Alveolar bone resorption was evaluated histologically. The expression profile of various genes was analyzed in gingival tissue, liver, small intestine and large intestine using real-time polymerase chain reaction. Sera were analyzed for antibody, endotoxin and interleukin (IL)-6 levels. Antibody levels were also analyzed for culture supernatant of cells from mesenteric lymph nodes and spleens. A proportion of T-helper 17 and Treg in the cells from mesenteric lymph nodes and spleens was analyzed by flow cytometry. The level of IL-6 and IL-17 in the cell culture supernatants was analyzed by enzyme-linked immunosorbent assay.
Results:
P. gingivalis administration did not induce alveolar bone resorption. Although P. gingivalis elicited systemic antibody response in germ-free mice, unlike in specific pathogen-free mice, P. gingivalis did not induce an inflammatory response in gingiva, liver and intestinal tissue, or alter the proportion of T-helper 17 and Treg. However, IL-6 and IL-17 productions were significantly elevated and tended to be elevated, respectively, in the cells from mesenteric lymph nodes of P. gingivalis-administered mice. Interestingly, the expression of IL-10 and tight junction protein in the gingiva and intestine, respectively, was significantly upregulated in P. gingivalis-treated mice. Administration of L. salivarius elicited almost similar effects as P. gingivalis.
Conclusion:
The oral pathobiont P. gingivalis did not induce any detectable pathogenic changes or any major host responses when administered to germ-free mice. There may be indirect mechanisms for gut-mediated systemic effects by P. gingivalis.
Insights
Porphyromonas gingivalis, a bacterium linked to systemic diseases, did not cause harm in germ-free mice. Further research is needed to understand how this oral bacterium might indirectly affect the gut and cause systemic issues.
Area of Science:
- Microbiology
- Immunology
- Gastroenterology
Background:
- Periodontitis is linked to systemic diseases via oral bacteria affecting gut microbiota.
- The precise mechanism of Porphyromonas gingivalis (P. gingivalis) generating systemic effects from the gut remains unclear.
Purpose of the Study:
- To investigate the gut-mediated systemic effects of orally administered P. gingivalis in germ-free mice.
- To explore the potential role of P. gingivalis in altering gut microbiota and inducing systemic inflammation.
Main Methods:
- Germ-free mice were orally administered P. gingivalis or Lactobacillus salivarius.
- Gene expression in gingival tissue, liver, and intestines was analyzed.
- Serum, mesenteric lymph node, and spleen cells were analyzed for immune markers (IL-6, IL-17, antibodies, T-helper cells).
Main Results:
- P. gingivalis did not induce alveolar bone resorption or local inflammation in germ-free mice.
- Systemic antibody response to P. gingivalis was observed, but without significant systemic inflammation.
- Elevated IL-6 and IL-17 in mesenteric lymph node cells and upregulated IL-10 and tight junction protein expression were noted.
Conclusions:
- P. gingivalis did not induce overt pathogenic changes or major host responses in germ-free mice.
- The study suggests potential indirect mechanisms for gut-mediated systemic effects by P. gingivalis.
- Further investigation is required to elucidate the exact pathways involved.
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