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A more recent version of this article appeared on November 1, 2007

Published online before print July 26, 2007
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0307160

Received for publication March 14, 2007.
Revised June 20, 2007.
Accepted for publication July 6, 2007.

Article

{beta}-Glucan of Candida albicans cell wall causes the subversion of human monocyte differentiation into dendritic cells

Roberto Nisini *@, Antonella Torosantucci *, Giulia Romagnoli {dagger}, Paola Chiani , Simona Donati {dagger}, Maria Cristina Gagliardi *, Raffaela Teloni *, Valeria Sargentini *, Sabrina Mariotti *, Egidio Iorio {dagger}, and Antonio Cassone *

*Dipartimento di Malattie Infettive, Parassitarie e Immunomediate; and {dagger}Dipartimento Biologia Cellulare e Neuroscienze. Istituto Superiore di Sanità, Rome, Italy

@ To whom correspondence should be addressed. E-mail: roberto.nisini{at}iss.it.


  Abstract

The functional consequences of treating human monocytes with purified and chemically characterized Candida albicans {beta}-glucan—a major microbial pathogen associated molecular pattern—on their differentiation into dendritic cells (DC) were investigated. We show here that {beta}-glucan-treated monocytes differentiated into mature DC (Glu-MoDC) with altered phenotype and functional behavior, similarly to DC derived from C. germ-tubes-infected monocytes (Gt-MoDC). They failed to express CD1a and to up-regulate CD80 and DR molecules. Moreover, they produced IL-10 but not IL-12 and primed naive T cells without inducing their functional polarization into effector cells. Since C. albicans {beta}-glucan is a mixture of both {beta}-(1,3) and {beta}-(1,6) glucan, we investigated their relative contribution by the use of non-Candida {beta}-glucan structural analogs. We found that high molecular weight (MW) glucans {beta}-(1,6) pustulan and {beta}-(1,3) curdlan totally mimicked the effect of C. albicans {beta}-glucan, while the low MW {beta}-(1,3) glucan laminarin did not have any effect. Because {beta}-glucan is a common constituent of all fungi and is abundantly released in vivo during systemic fungal infection, this novel effect of {beta}-glucan has potential implications for a host-parasite relationship in candidiasis and other mycoses. In particular, our data suggest that {beta}-glucan could bias noninfected, bystander monocytes, thus aggravating the general immunodeficiency, predisposing them to systemic fungal infection.

Key Words: fungi • antigen presentation/processing • {beta}-glucan structure






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Copyright © 2007 by the Society for Leukocyte Biology.