Alteration of ascending colon mucosal microbiota in patients after cholecystectomy

BACKGROUND Cholecystectomy is a successful treatment option for gallstones,although the inci-dence of colorectal cancer(CRC)has notably increased in post-cholecystectomy(PC)patients.However,it remains uncertain whether the altered mucosal micro-biota in the ascending colon is related.In total,30 PC patients and 28 healthy controls underwent colonoscopies to collect mucosal biopsy samples.PC patients were divided based on their clinical features.Then,16S-rRNA gene sequencing was used to analyze the amplicon,alpha diversity,beta diversity,and composition of the bacterial communities.Addi-tionally,the Phylogenetic Investigation of Communities by Reconstruction of Unobserved States(PICRUSt)database,sourced from the Kyoto Encyclopedia of Genes and Genomes,was used to predict the functional capabilities of the bac-teria.RESULTS PC patients were comparable with healthy controls.However,PC patients older than 60 years had a distinct composition compared to those under 60 years old.Bacteroidetes richness was considerably higher at the phylum level in PC patients.Bacteroides,Parabacteroides,and Bilophila were more abundant in the PC group than in the control group.Furthermore,PC patients exhibited greater enrichment in metabolic pathways,specifically those related to lipopolysaccharide biosynthesis and vancomycin group antibiotic production,than controls.CONCLUSION This study indicated that the mucosal microbiota in PC patients was altered,perhaps offering new perspectives on the treatment possibilities for CRC and diarrhea following cholecystectomy.

Fusobacterium nucleatum promotes colon cancer progression by changing the mucosal microbiota and colon transcriptome in a mouse model

BACKGROUND Fusobacterium nucleatum(F.nucleatum)has long been known to cause opportunistic infections and has recently been implicated in colorectal cancer(CRC),which has attracted broad attention.However,the mechanism by which it is involved in CRC development is not fully understood.AIM To explore its potential causative role in CRC development,we evaluated the colon pathology,mucosa barrier,colon microbiota and host transcriptome profile after F.nucleatum infection in an azoxymethane/dextran sulfate sodium salt(AOM/DSS)mouse model.METHODS Three groups of mice were compared to reveal the differences,i.e.,the control,AOM/DSS-induced CRC and AOM/DSS-FUSO infection groups.RESULTS Both the AOM/DSS and AOM/DSS-FUSO groups exhibited a significantly reduced body weight and increased tumor numbers than the control group,and AOM/DSS mice with F.nucleatum infection showed the highest tumor formation ratio among the three groups.Moreover,the colon pathology was the most serious in the AOM/DSS-FUSO group.We found that the structure of the colon microbiota changed considerably after F.nucleatum infection;striking differences in mucosal microbial population patterns were observed between the AOM/DSS-FUSO and AOM/DSS groups,and inflammation-inducing bacteria were enriched in the mucosal microbiota in the AOM/DSS-FUSO group.By comparing intestinal transcriptomics data from AOM vs AOM/DSSFUSO mice,we showed that transcriptional activity was strongly affected by dysbiosis of the gut microbiota.The most microbiota-sensitive genes were oncogenes in the intestine,and the cyclic adenosine monophosphate signaling pathway,neuroactive ligand–receptor interaction,PPAR signaling pathway,retinol metabolism,mineral absorption and drug metabolism were highly enriched in the AOM/DSS-FUSO group.Additionally,we showed that microbial dysbiosis driven by F.nucleatum infection enriched eight taxa belonging to Proteobacteria,which correlates with increased expression of oncogenic genes.CONCLUSION Our study demonstrated that F.nucleatum infection altered the colon mucosal microbiota by enriching pathogens related to the development of CRC,providing new insights into the role of F.nucleatum in the oncogenic microbial environment of the colon.

The development and role of microbialhost interactions in gut mucosal immune development

At birth the piglet＇s immune system is immature and it is dependent upon passive maternal protection until weaning.The piglet＇s mucosal immune system develops over the first few weeks but has not reached maturity at weaning ages which are common on commercial farms. At weaning piglets are presented with a vast and diverse range of microbial and dietary/environmental antigens. Their ability to distinguish between antigens and mount a protective response to potential pathogens and to develop tolerance to dietary antigens is critical to their survival and failure to do so is reflected in the high incidence of morbidity and mortality in the post-weaning period. A growing recognition that the widespread use of antibiotics to control infection during this critical period should be controlled has led to detailed studies of those factors which drive the development of the mucosal immune system, the role of gut microbiota in driving this process, the origin of the bacteria that colonise the young piglet＇s intestine and the impact of rearing environment. This review briefly describes how the mucosal immune system is equipped to respond ＂appropriately＂ to antigenic challenge and the programmed sequence by which it develops. The results of studies on the critical interplay between the host immune system and gut microbiota are discussed along with the effects of rearing environment. By comparing these with results from human studies on the development of allergies in children, an approach to promote an earlier maturation of the piglet immune system to resist the challenges of weaning are outlined.

Mucosa-associated microbiota alterations in primary sclerosing cholangitis(PSC)before and after liver transplantation-who is calling the shots?

Primary sclerosing cholangitis(PSC)is an immune-related chronic cholangiopathy associated with high rates of progression to liver cirrhosis and the need for liver transplantation.Since PSC is frequently associated with inflammatory bowel disease(IBD),several studies have investigated the role of the gut-liver axis in PSC and emerging evidence indicates that gut and bile microbiota are associated with the onset and progression of PSC[reviewed in(1)].