Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Changes of Gut Microbiota in Fap and UC Patients in Mediteranean Region of Turkey: An –Omic Landscape to Be Discovered

Version 1 : Received: 15 December 2020 / Approved: 16 December 2020 / Online: 16 December 2020 (18:05:43 CET)

How to cite: HANTA, A.; Rencuzogullari, A.; Boga, I.; Eray, I.C.; Bisgin, A. Changes of Gut Microbiota in Fap and UC Patients in Mediteranean Region of Turkey: An –Omic Landscape to Be Discovered. Preprints 2020, 2020120416 (doi: 10.20944/preprints202012.0416.v1). HANTA, A.; Rencuzogullari, A.; Boga, I.; Eray, I.C.; Bisgin, A. Changes of Gut Microbiota in Fap and UC Patients in Mediteranean Region of Turkey: An –Omic Landscape to Be Discovered. Preprints 2020, 2020120416 (doi: 10.20944/preprints202012.0416.v1).

Abstract

Inflammatory bowel diseases, familial adenomatous polyposis (FAP) and colorectal cancer (CRC) are associated with alterations of the intestinal microbiota. However, few data are available on the perpetuation of FAP and ulcerative colitis (UC) in relation to microbial dysbiosis. This study evaluated the UC and genetically confirmed FAP patients’ gut microbial balance in concordance to clinical outcome. Fecal materials (average mass of 0.54 g) were collected from three FAP and five UC patients to compare with healthy individuals as control group. Genomic materials of micro-biota were isolated for next generation sequencing of 16S rRNA that was performed by using QIAseq 16S/ITS panel in Illumina Miseq Platform. Data processing and bioinformatics analysis were performed via CLC Genomic Workbench bioinformatics tool. The comparison between FAP, UC and control group revealed an alteration in the intestinal microbial composition. More in details, relative abundance of class levels showed statistical significance differences among FAP, UC and control groups. Our preliminary data focused on the explanation of how dysbiosis can lead to inflammation and drive processes together with host genetic profile that leads to colorectal carcinogenesis.

Keywords

dysbiosis; familial adenomatous polyposis,; ulcerative colitis; 16S rRNA; gut microbiota; geo-graphic populations

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