d The tumor size distribution in the intestine was listed and compared with control-FMT (n?=?8 for each group). prevention. Methods Here, we used C57BL/6?J mice, an animal model of human intestinal tumorigenesis, GW627368 to investigate the gut bacterial diversity and their mechanisms of action in gastrointestinal adenomas, and to evaluate the effects of Yi-Yi-Fu-Zi-Bai-Jiang-San (YYFZBJS) on of colon carcinogenesis in vivo and in vitro. Through human-into-mice fecal microbiota transplantation (FMT) experiments from YYFZBJS volunteers or control donors, we were able to differentially modulate the tumor microbiome and affect tumor growth as well as tumor immune infiltration. Results We report herein, YYFZBJS treatment blocked tumor initiation and progression in mice with less change of body weight and increased immune function. Moreover, diversity GW627368 analysis of fecal samples exhibited that YYFZBJS regulated animals natural gut flora, including and so on. Intestinal tumors from conventional and germ-free mice fed with stool from YYFZBJS volunteers had been decreased. Some inflammation expression also have been regulated by the gut microbiota mediated immune cells. Intestinal lymphatic, and mesenteric lymph nodes (MLN), accumulated CD4+ CD25+ Foxp3 positive Treg cells were reduced by YYFZBJS treatment in mice. Although YYFZBJS had no inhibition on CRC cell proliferation by itself, the altered Tregs mediated by YYFZBJS repressed CRC cancer cell growth, along with reduction of the phosphorylation of -catenin. Conclusions In conclusion, we exhibited that gut microbiota and Treg were involved in CRC development and progression, and we propose YYFZBJS as a new potential drug option for the treatment of CRC. Video abstract video file.(43M, mp4) Graphical abstract mice, Gut microbiota, Fecal microbiota transplantation, Regulatory T cell, Immune, Traditional Chinese herb medicine Background CRC is one of the most common cancers with an annual incidence of nearly 1 million cases worldwide and an GW627368 annual mortality of more than 600,000 patients . Accumulating evidence suggests that the gut microbiota, chronic inflammation, host genetic predisposition, and environmental factors have been linked with the progression of CRC . GW627368 Previous studies have identified several bacteria that can promote carcinogenesis by different mechanisms, such as Bacteroides, which can Rabbit Polyclonal to DUSP22 alter bile acid metabolism and/or increase IL-22 levels ; Fusobacterium nucleatum which can activate the autophagy pathway and alter colorectal cancer chemotherapeutic response through Toll-like receptor pathways  and Eschericia which can induce colonic contamination in the bacterial mediated CRC . Interestingly, the fecal samples of CRC patients can induce intestinal tumorigenesis and colon cell proliferation in colon tumour model mice, as well as increase the expression of inflammatory genes and carcinogenic factors . Fecal microbiota transplantation (FMT) is usually one procedure that involves the complete restoration of the entire fecal microbiota instead of a single agent or combination of brokers. Emerging studies have found significant differences in intestinal microbial communities between CRC patients and healthy individuals . A key player involved in the processes of gut microbiota and tumorigenesis is the tumor-infiltrating immune cell, which is popular in the intestinal tract and contains a myriad of immune cells, such as macrophages, dendritic cells, neutrophils, and lymphocytes (T cells), start from naive T cells to undergo differentiation processes during which they acquire the capacity to produce distinct sets of effector cytokines . Different lineages derived from CD4+ T cells including Th1, Th2, Th17, regulatory T, and Tr1 cells, have extensive effects in cancer development. Current studies have mainly explored the changes of the circulating levels of cytokines that reflect the balance of the four T cells, i.e. plasma levels of interferon gamma (IFN-), interleukin-6/10 (IL-6/10), and tumor necrosis factor- (TNF-)] [9, 10]. In recent years, clinical observations indicated that CD4+ CD25+ regulatory T cells (Tregs) played a promoting role in various cancers such as gastric, colorectal, pancreatic cancers and hepatocellular carcinoma [11C13]. Moreover, Tregs was reported to suppress immune responses and hinder suppression of tumor growth in preclinical models . Emerging studies have highlighted a key role for the commensal microbiota in the immunoregulatory responses, probably through GW627368 affecting T-helper (TH) and T regulatory cells (Tregs) . For example, together with a tryptophan-rich diet.