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Bacterial translocation in cirrhosis is not caused by an abnormal small bowel gut microbiota.

Authors :
Steed H
Macfarlane GT
Blackett KL
Macfarlane S
Miller MH
Bahrami B
Dillon JF
Source :
FEMS immunology and medical microbiology [FEMS Immunol Med Microbiol] 2011 Dec; Vol. 63 (3), pp. 346-54. Date of Electronic Publication: 2011 Sep 08.
Publication Year :
2011

Abstract

Sepsis is common in liver cirrhosis, and animal studies have shown the gut to be the principal source of infection, through bacterial overgrowth and translocation in the small bowel. A total of 33 patients were recruited into this study, 10 without cirrhosis and 23 with cirrhotic liver disease. Six distal duodenal biopsies were obtained and snap frozen for RNA and DNA extraction, or frozen for FISH. Peripheral venous bloods were obtained from 30 patients, including 17 chronic liver disease patients. Samples were analysed by real-time PCR, to assess total bacteria, bifidobacteria, bacteroides, enterobacteria, staphylococci, streptococci, lactobacilli, enterococci, Helicobacter pylori and moraxella, as well as TNF-α, IL-8 and IL-18. There was no evidence of bacterial overgrowth with respect to any of the individual bacterial groups, with the exception of enterococci, which were present in higher numbers in cirrhotic patients (P = 0.04). There were no significant differences in any of the cytokines compared to the controls. The small intestinal mucosal microbiota in cirrhotic patients was qualitatively and quantitatively normal, and this shifts the focus of disease aetiology to factors that reduce gut integrity, failure of mechanisms to remove translocating bacteria, or the large bowel as the source of sepsis.<br /> (© 2011 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved.)

Details

Language :
English
ISSN :
1574-695X
Volume :
63
Issue :
3
Database :
MEDLINE
Journal :
FEMS immunology and medical microbiology
Publication Type :
Academic Journal
Accession number :
22092561
Full Text :
https://doi.org/10.1111/j.1574-695X.2011.00857.x