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Sci Rep ; 9(1): 10923, 2019 07 29.
Article in English | MEDLINE | ID: mdl-31358825

ABSTRACT

The dysbiosis of human gut microbiota is strongly associated with the development of colorectal cancer (CRC). The dysbiotic features of the transition from advanced polyp to early-stage CRC are largely unknown. We performed a 16S rRNA gene sequencing and enterotype-based gut microbiota analysis study. In addition to Bacteroides- and Prevotella-dominated enterotypes, we identified an Escherichia-dominated enterotype. We found that the dysbiotic features of CRC were dissimilar in overall samples and especially Escherichia-dominated enterotype. Besides a higher abundance of Fusobacterium, Enterococcus, and Aeromonas in all CRC faecal microbiota, we found that the most notable characteristic of CRC faecal microbiota was a decreased abundance of potential beneficial butyrate-producing bacteria. Notably, Oscillospira was depleted in the transition from advanced adenoma to stage 0 CRC, whereas Haemophilus was depleted in the transition from stage 0 to early-stage CRC. We further identified 7 different CAGs by analysing bacterial clusters. The abundance of microbiota in cluster 3 significantly increased in the CRC group, whereas that of cluster 5 decreased. The abundance of both cluster 5 and cluster 7 decreased in the Escherichia-dominated enterotype of the CRC group. We present the first enterotype-based faecal microbiota analysis. The gut microbiota of colorectal neoplasms can be influenced by its enterotype.


Subject(s)
Adenoma/microbiology , Colorectal Neoplasms/microbiology , Gastrointestinal Microbiome , Adenoma/pathology , Aeromonas/genetics , Aeromonas/pathogenicity , Aged , Bacteroidaceae/genetics , Bacteroidaceae/pathogenicity , Colorectal Neoplasms/pathology , Enterococcus/genetics , Enterococcus/pathogenicity , Escherichia/genetics , Escherichia/pathogenicity , Female , Fusobacterium/genetics , Fusobacterium/pathogenicity , Haemophilus/genetics , Haemophilus/pathogenicity , Humans , Male , Middle Aged , RNA, Ribosomal, 16S/genetics
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