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Colonisation by F aecalibacterium prausnitzii and maintenance of clinical remission in patients with ulcerative colitis
Author(s) -
Varela E.,
Manichanh C.,
Gallart M.,
Torrejón A.,
Borruel N.,
Casellas F.,
Guarner F.,
Antolin M.
Publication year - 2013
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1111/apt.12365
Subject(s) - faecalibacterium prausnitzii , ulcerative colitis , medicine , gastroenterology , calprotectin , colitis , feces , immunology , inflammatory bowel disease , gut flora , microbiology and biotechnology , disease , biology
Summary Background Although incrimination of the intestinal microbiota in the pathogenesis of IBD is widely accepted, few data are available about the role of specific bacteria. Potentially, F aecalibacterium prausnitzii , bacteria with anti‐inflammatory properties, might be deficient in ulcerative colitis ( UC ). Aim To quantify F . prausnitzii in the faecal microbiota of UC patients in remission and determine its relationship with relapse. Methods A cross‐sectional study included 116 UC patients in remission, 29 first‐degree relatives and 31 healthy controls. A subset of eighteen patients, recruited during the first month of remission, underwent a 1‐year follow‐up. Total bacteria and F . prausnitzii were measured by quantitative Real Time PCR ( qPCR , copies/g). Calprotectin was determined as inflammatory index (μg/g). Results We found that F . prausnitzii was reduced in patients (median, IQR : 1.4 × 10 8 , 5.1 × 10 7 –4.5 × 10 8 ) and relatives (1.7 × 10 8 , 9.3 × 10 7 –5.1 × 10 8 ) vs. controls (6.5 × 10 8 , 3.7 × 10 8 –1.6 × 10 9 , P < 0.0001). Moreover, low counts of F . prausnitzii were associated with less than 12 months of remission (8.0 × 10 7 , 2.0 × 10 7 –3.5 × 10 8 vs. 2.1 × 10 8 , 1.0 × 10 8 –7.9 × 10 8 , P < 0.001) and more than 1 relapse/year (8.0 × 10 7 , 3.2 × 10 7 –3.8 × 10 8 vs. 1.9 × 10 8 , 6.8 × 10 7 –6.0 × 10 8 , P < 0.01). When patients were followed up, F . prausnitzii increased steadily until reaching similar levels to those of controls if remission persisted (2.9 × 10 8 , 9.3 × 10 6 –1.2 × 10 9 ; calprotectin: 76, 19–212), whereas it remained low if patients relapsed (2.2 × 10 8 , 1.4 × 10 6 –3.3 × 10 8 ; calprotectin: 1760, 844–3662 P < 0.05 vs. controls). Conclusions Defective gut colonisation by F . prausnitzii occurred in UC patients during remission and in their unaffected relatives. The recovery of the F . prausnitzii population after relapse is associated with maintenance of clinical remission.