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Table of Contents
Vol. 27, Suppl. 1, 2009
Issue release date: March 2010
Section title: Paper
Dig Dis 2009;27(suppl 1):104–110
(DOI:10.1159/000268129)

Yeasts: Neglected Pathogens

Poulain D. · Sendid B. · Standaert-Vitse A. · Fradin C. · Jouault T. · Jawhara S. · Colombel J.-F.
Université Lille Nord de France, UDSL, CHU Lille, Inserm U799, Inserm U795, Lille, France

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Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: March 04, 2010
Issue release date: March 2010

Number of Print Pages: 7
Number of Figures: 3
Number of Tables: 0

ISSN: 0257-2753 (Print)
eISSN: 1421-9875 (Online)

For additional information: http://www.karger.com/DDI

Abstract

Background: Current research on Crohn’s disease (CD) concerns molecular events related to loss of tolerance to microbes that could trigger or maintain inflammation in genetically susceptible individuals. CD is also associated with antimicrobial antibodies, including the antibodies we described against yeast oligomannosides (ASCA). This prompted us to investigate a role for another yeast, Candida albicans, a very common commensal of the human digestive tract and an important opportunistic pathogen. Clinical and Experimental Data: It has been revealed that the major oligomannose epitopes supporting ASCA are expressed by C. albicans in human tissues, suggesting that C. albicans is the immunogen for ASCA. This link has been reinforced by the demonstration that novel serological markers of CD (ALCA and ACCA), consisting of antibodies against chitin and glucan (two components of the C. albicans cell wall), are also generated during C. albicans infection. Mycological investigation of families with multiple cases of CD shows that patients with CD and their healthy relatives are colonized with C. albicans more commonly than control families. In healthy relatives, C. albicans colonization correlates with ASCA levels, whereas the onset of CD is associated with ASCA stability and is independent of the C. albicans intestinal load. Experimental studies show that chemically-induced colitis promotes C. albicans colonization in mice. In turn, C. albicans colonization generates ASCA, increases inflammation, histological scores and pro-inflammatory cytokine expression. Perspectives: Current investigations focus on interactions of TLRs and lectins with yeast epitopes that differently polarize the immune response to C. albicans cell wall glycans, which are the targets of an ‘excessive’ adaptive response associated with CD.

© 2010 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: March 04, 2010
Issue release date: March 2010

Number of Print Pages: 7
Number of Figures: 3
Number of Tables: 0

ISSN: 0257-2753 (Print)
eISSN: 1421-9875 (Online)

For additional information: http://www.karger.com/DDI


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Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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