This is the authors' abstract. We don't add key points for this paper.
Porphyromonas gingivalis is associated with periodontal diseases, including gingivitis and periodontitis. P. gingivalis infiltrates the periodontal tissues, liberating various outer membrane vesicles, including lipopolysaccharides (LPSs). These vesicles trigger the innate immune response, thereby promoting inflammation. Therefore, LPS is commonly used to study microbiome infections and colonization dynamics. In this study, we identified a novel Canis familiaris gingival-derived microbiome associated with the reduction of PG-LPS. To investigate the effects of microbiome on the PG-LPS, we cultured RAW 264.7 macrophages and determined the expression patterns of inflammatory marker genes in PG-LPS-induced RAW 264.7 macrophages. Concentration of nitric oxide, an inflammatory marker, was decreased by the microbiome treatment. In addition, levels of inflammatory marker genes (interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha) were upregulated in the LPS-treated control cells while, downregulated in the microbiome and LPS co-treated RAW 264.7 cells. Our results suggest that the identified microbiome reduces PG-LPS derived inflammation; however, the underlying mechanism remains unclear. Therefore, future studies should explore the mechanisms underlying the candidate microbiome-mediated inflammation reduction.
No takes yet. Share an insight, caveat, or question.
Park et al. (2025) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: