Validation experiment designed to validate causal mechanisms targeting GPR109A in Germ-free mice with fecal microbiota transplantation. Primary outcome: GPR109A suppression and barrier dysfunction in recipient mice
This experiment utilized germ-free mice as recipients for fecal microbiota transplantation to directly test the role of periodontitis-associated gut microbiota in mediating intestinal dysfunction. Fecal microbiota from control mice (GF-CON) and ligature-treated mice with periodontitis (GF-LIG) were transplanted into germ-free recipients. The study then analyzed colonic GPR109A levels, tight junction integrity, and inflammatory responses in the recipient mice. This approach allowed for direct causal testing of whether the altered microbiota composition from periodontitis donors could recapitulate the intestinal pathology observed in the original periodontitis model, thereby confirming a microbiota-dependent mechanism.
Fecal microbiota transplantation from control and periodontitis donor mice into germ-free recipients, followed by analysis of GPR109A expression, tight junction proteins, and inflammatory markers
Microbiota from periodontitis donors would suppress GPR109A and induce barrier dysfunction
Significant GPR109A suppression, tight junction impairment, and inflammatory upregulation in recipients of periodontitis microbiota
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