Open AccessBacterial translocation in cirrhosis is not caused by an abnormal small bowel gut microbiota
Author(s) -
Steed Helen,
Macfarlane George T.,
Blackett Katie L.,
Macfarlane Sandra,
Miller Michael H.,
Bahrami Bahram,
Dillon John F.
Publication year - 2011
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.2011.00857.x
Subject(s) - biology , cirrhosis , gastroenterology , bacteroides , gut flora , sepsis , fusobacterium , medicine , inflammatory bowel disease , microbiology and biotechnology , immunology , bacteria , disease , genetics
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.