Implication of Porphyromonas gingivalis in colitis and homeostasis of intestinal epithelium

Abstract

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.

Superoxide Dismutase 3-Transduced Mesenchymal Stem Cells Preserve Epithelial Tight Junction Barrier in Murine Colitis and Attenuate Inflammatory Damage in Epithelial Organoids

“…To generate intestinal organoids (IOs), intestinal crypts were isolated from the mouse small intestine as previously described [ 53 , 54 ]. In brief, the harvested mouse small intestine was longitudinally opened and villi were removed by gentle scraping with a glass coverslip.…”

The Link between Oral and Gut Microbiota in Inflammatory Bowel Disease and a Synopsis of Potential Salivary Biomarkers

“…To date, over 700 oral bacterial species have been identified in the human oral microbiome database (HOMD) [94]. Saliva, shedding of soft surfaces, buccal mucosa, palatal mucosa, tongue dorsum, and supragingival plaque contribute to the oral microbiome [95,96]. Likewise, hard and mucosal surfaces within the oral cavity maintain environments suitable for commensal bacteria to flourish and protect the integrity of the gingival and epithelial cells [96].…”

“…Saliva, shedding of soft surfaces, buccal mucosa, palatal mucosa, tongue dorsum, and supragingival plaque contribute to the oral microbiome [95,96]. Likewise, hard and mucosal surfaces within the oral cavity maintain environments suitable for commensal bacteria to flourish and protect the integrity of the gingival and epithelial cells [96]. Similar to other regions of the digestive tract, the oral cavity is subject to constant environmental exposures that may impact pH, temperature, oxygen, and available nutrients due to continuous exposure to environmental insults such as food, beverage, and potential pathogens.…”

Xeno-Free Condition Enhances Therapeutic Functions of Human Wharton’s Jelly-Derived Mesenchymal Stem Cells against Experimental Colitis by Upregulated Indoleamine 2,3-Dioxygenase Activity

“…We explored whether the systemic administration of WJ-MSCs rescued mice from dextran sulfate sodium (DSS)-induced colitis and whether XF culture conditions enhanced the protective effect of WJ-MSCs against colitis ( Figure 7 A). The mice treated with 3% DSS solution exhibited clinical signs of colitis, including sustained weight loss, diarrhea, and bloody stools [ 34 ]. Intraperitoneal injections of WJ-MSCs ameliorated body weight loss and increased the survival rate of mice compared to the positive control group ( Figure 7 B,C).…”