Epigallocatechin gallate protects mice from Salmonella enterica ser. Typhimurium infection by modulating bacterial virulence through quorum sensing inhibition.

Salmonella enterica ser. Typhimurium is a common pathogen that poses a considerable public health threat, contributing to severe gastrointestinal diseases and widespread foodborne illnesses. The virulence of S. Typhimurium is regulated by quorum sensing (QS) and the type III secretion system (T3SS). This study investigated the inhibitory effects and anti-QS activity of epigallocatechin gallate (EGCG), which is a bioactive ingredient found in green tea, on the virulence of S. Typhimurium. In vitro bacterial experiments demonstrated that EGCG inhibited the production of autoinducers, biofilm formation, and flagellar activity by downregulating the expression of AI-1, AI-2, Salmonella pathogenicity islands (SPI)-1, SPI-2, and genes related to flagella, fimbriae, and curli fibers. In a mouse model of S. Typhimurium-induced enteritis, EGCG considerably reduced intestinal colonization by S. Typhimurium and alleviated intestinal damage. In conclusion, EGCG protects the intestines of mice infected with S. Typhimurium by inhibiting QS-induced virulence gene expression, demonstrating its potential as a therapeutic agent for controlling S. Typhimurium infections.

Study on the function of Huazhuo Jiedu Decoction in promoting the homing of bone marrow mesenchymal stem cells and contributing to the treatment of ulcerative colitis.

Objective: To study the function of Huazhuo Jiedu Decoction (HZJD) in promoting the homing of bone marrow mesenchymal stem cells (BMSCs) and contributing to the reconstruction of the intestinal mucosal barrier in ulcerative colitis. Methods: Bone mesenchymal stem cells derived from mice were isolated and cultured, osteogenic and adipogenic assays to study the differentiation ability of BMSCs, and flow cytometry was used to detect the surface marker of the third generation cells. 30 mice were selected and divided into blank group, model group, HZJD group, BMSCs group, and HZJD combined with BMSCs group. Mouse colon length, body weight, and DAI score were used to assess efficacy. The levels of IL-6, IL-1ß, TNF-α, and IFN-γ in serum were measured by ELISA. BMSCs transfected with GFP were used to mark the homing of BMSCs in mice. The BMSCs tagging protein CD90+/CD29+ was detected by immunofluorescence. H&E staining detects damage to the colon and the inflammatory response. The expression levels of claudin-2, claudin-4, occludin, and ZO-1 in colon tissues were detected by Western blot. Results: After subculture, the cell grew with adherence. Flow cytometry showed that the cells were CD73+/CD90+/CD29+/CD45-/CD34-, which belonged to bone mesenchymal stem cells. ELISA showed that the treatment with HZJD and BMSCs suppressed the DSS-induced inflammatory response. BMSCs carrying GFP can be detected in intestinal tissues. Immunofluorescence showed that the HZJD combined with the BMSCs group had more BMSCs homing to the colonic tissue. The results of H&E and Western blot showed that DSS-induced intestinal mucosal damage in UC mice was repaired by HZJD and BMSCs, and the abnormal tight junction proteins claudin-2, claudin-4, occludin, and ZO-1 were normalized. Conclusion: HZJD has a therapeutic effect on ulcerative colitis by promoting the migration of BMSCs to ulcers of the colon and contributing to the reconstruction of the intestinal mucosal barrier in ulcerative colitis.