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J Infect Dis. 2008 Apr 1;197(7):972-80. doi: 10.1086/528990.

Colonization of mice by Candida albicans is promoted by chemically induced colitis and augments inflammatory responses through galectin-3.

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Inserm U 799, Physiopathologie des Candidoses, Faculté de Médecine, Centre Hospitalier Régional Universitaire de Lille, Institut Fédératif de Recherche 114, Université Lille 2, , Lille, France.



Little is known about the relationship between colonic inflammation and Candida albicans colonization. Galectin-3 (Gal-3) is an intestinal lectin that binds to specific C. albicans glycans and is involved in inflammation.


Colitis was experimentally induced in wild-type and Gal3(-/-) mice using dextran sulfate sodium (DSS) before oral administration of C. albicans. Yeast recovered from stools was quantified. The presence of yeast and inflammation were evaluated in sections of colon by histologic examination, quantification of myeloperoxidase (MPO) activity, and by gene expression for cytokines and innate immune receptors. Serum from mice was collected for determination of anti-yeast mannan antibodies, including anti-Saccharomyces cerevisiae antibodies (ASCA), which are biomarkers of an inflammatory bowel disease.


Inflammation strongly promoted C. albicans colonization. Conversely, C. albicans augmented inflammation induced by DSS, as assessed by histologic scores, MPO activity, and tumor necrosis factor (TNF)-alpha and Toll-like receptor (TLR)-2 expression. C. albicans colonization generated ASCA. The absence of Gal-3 reduced DSS inflammation and abolished the response of TLR-2 and TNF-alpha to C. albicans colonization.


DSS-induced colitis provides a model for establishing C. albicans colonization in mice. This model reveals that C. albicans augments inflammation and confirms the role of Gal-3 in both inflammation and the control of host responses to C. albicans.

[Indexed for MEDLINE]

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