Emerging evidences have reported that
periodontitis can be a
risk factor for the pathogenesis of various systemic
diseases.
Porphyromonas gingivalis (Pg), one of the crucial pathogens in
chronic periodontitis, has been spotlighted as a potential cause for the promotion and
acceleration of
periodontitis-associated systemic disorders. To investigate the
association between Pg and
intestinal disease or
homeostasis, we treated Pg-derived
lipopolysaccharide (LPS) in murine
colitis model or intestinal
organoid, respectively. Pg-derived LPS (Pg LPS) was administrated into
chemically induced murine
colitis model and
disease symptoms were monitored compared with the infusion of LPS derived from E. coli (Ec LPS).
Organoids isolated and cultured from
mouse small intestine were treated with Pg or Ec LPS and further analyzed for the generation and composition of
organoids. In vivo observations demonstrated that both Pg and Ec LPS exerted slight protective effects against murine
colitis. Pg LPS did not
affect the generation and
growth of intestinal epithelial
organoids. Among subtypes of
epithelial cells, markers for
stem cells,
goblet cells or
Paneth cells were changed in response to Pg LPS. Taken together, these results indicate that Pg LPS leads to partial improvement in
colitis and that its
treatment does not significantly
affect the
self-
organization of intestinal
organoids but may regulate the epithelial composition.