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

Helen Steed, George T. Macfarlane, Katie L. Blackett, Sandra Macfarlane, Michael H. Miller, Bahram Bahrami, John F. Dillon

    Research output: Contribution to journalArticlepeer-review

    20 Citations (Scopus)

    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-a, 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 similar to=similar to 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.

    Original languageEnglish
    Pages (from-to)346-354
    Number of pages9
    JournalFEMS Immunology and Medical Microbiology
    Volume63
    Issue number3
    DOIs
    Publication statusPublished - Dec 2011

    Keywords

    • cirrhosis
    • bacterial overgrowth
    • small bowel
    • chronic liver disease
    • REAL-TIME PCR
    • TARGETED OLIGONUCLEOTIDE PROBES
    • IN-SITU HYBRIDIZATION
    • 16S RIBOSOMAL DNA
    • AMINO-ACIDS
    • INTESTINAL PERMEABILITY
    • HEPATIC-ENCEPHALOPATHY
    • ULCERATIVE-COLITIS
    • COLONIC BACTERIA
    • FECAL SAMPLES

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