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World J Gastroenterol. Jan 14, 2006; 12(2): 292-297
Published online Jan 14, 2006. doi: 10.3748/wjg.v12.i2.292
Correlation between Saccharomyces cerevisiae DNA in intestinal mucosal samples and anti-Saccharomyces cerevisiae antibodies in serum of patients with IBD
RC Mallant-Hent, M Mooij, BME von Blomberg, RK Linskens, AA van Bodegraven, PHM Savelkoul
RC Mallant-Hent, AA van Bodegraven, Department of Gastroenterology, VU University Medical Center, Amsterdam, The Netherlands
M Mooij, PHM Savelkoul, Department of Medical Microbiology and Infection Control, VU University Medical Center, Amsterdam, The Netherlands
BME von Blomberg, Department of Immunology, VU University Medical Center, Amsterdam, The Netherlands
RK Linskens, Department of Gastroenterology, St Anna Ziekenhuis, Geldrop, The Netherlands
Correspondence to: Adriaan A van Bodegraven, Department of Gastroenterology, Small Bowel Disease Unit, VU University Medical Center, Postbox 7057, 1007 MB Amsterdam, The Netherlands. v.bodegraven@vumc.nl
Telephone: +31-20-4440613 Fax: +31-20-4440554
Received: June 3, 2005
Revised: June 8, 2005
Accepted: June 24, 2005
Published online: January 14, 2006
Abstract

AIM: To investigate the correlation between ASCA and presence of mucosal S. cerevisiae DNA in a population of CD, ulcerative colitis (UC) patients and controls.

METHODS: S. cerevisiae-specific primers and a fluorescent probe were designed for a 5’ exonuclease real time PCR (TaqManTM) assay, which is a homogenous system using a fluorescent-labelled probe for the detection of PCR product in real time. We analyzed the relation of the PCR results with the ASCA findings in a group of 76 inflammatory bowel disease (IBD) patients (31 CD, 45 UC) and 22 healthy controls (HC).

RESULTS: ASCA (IgA or IgG) were positive in 19 (61%) patients with CD, 12 (27%) with UC and none of the HC. PCR amplification was inhibited and excluded from the final results in 10 (22%) UC patients, 7 (22%) CD patients, and 6 (30%) HC. In only 15 of the mucosal samples, S. cerevisiae DNA was detected by real time PCR, including 7 (29%) in CD, 7 (19%) in UC, 1 (6%) in HC. In 4 CD and in 4 UC patients, ASCA and mucosal S. cerevisiae were positive. Mucosal S. cerevisiae was present in combination with negative ASCA IgA and IgG in 3 UC, and 3 CD patients.

CONCLUSION: We conclude that since the presence of S. cerevisiae in colonic mucosal biopsy specimens is very rare, ASCA is unlikely to be explained by continuous exposure to S. cerevisiae in the mucosa. Therefore, ASCA formation must occur earlier in life and levels remain relatively stable thereafter in immunological susceptible persons.

Keywords: ASCA; Saccharomyces cerevisiae; mucosa; IBD