作者: Laura Morris
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摘要: Introduction:-The human gut microbiota outnumbers our own cells by 100-1 and is often considered an extension of genome harboring fundamental functions which we are genetically incapable. However, it can also be a significant liability has been implicated in numerous diseases, particularly; Inflammatory Bowel Disease (IBD). The efforts this research entailed evaluating specific molecular mechanism the bacterial metagenome; proteolytic activity, collectively known as Degradome due to their putative role virulence factors IBD. In order access degradome microbiota, firstly, novel functional metagenomic (FM) tools were developed with aim facilitating isolation proteases. Secondly, comprehensive cohort study was conducted comparing faecal protease 16S rRNA microbial community structure potential act between group IBD patients healthy volunteers begin determine proteases disease aetiology. Results:-The exhibited significantly higher activity than cohort. Inhibitor assays showed that contained different types levels metalloprotease activity. gene analysis revealed dysbiosis Dysbiosis observed high producers low able decrease trans epithelial resistance HT-29 cell line increase cellular permeability. Functional metagenomics assessed for from microbiota. ability deficient strain; Bacillus subtilis WB800N express compared E. coli its usefulness host FM screening B. gelatinase E neutral while not suggesting more suitable host. when screened using host, none isolated improvements still needed made. Conclusions: - Compositional alterations appear associated had elevated expanded repertoire have factor disrupting barrier integrity. Proteases remain elusive via screening; however highlighted areas need improvement optimize future screens accessing