Journal of Leukocyte Biology eBioscience full spectrum cell analysis
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Originally published online as doi:10.1189/jlb.0307160 on July 26, 2007

Published online before print July 26, 2007
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(Journal of Leukocyte Biology. 2007;82:1136-1142.)
© 2007 by Society for Leukocyte Biology

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

Roberto Nisini*,1, 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

1 Correspondence: Dipartimento di Malattie Infettive, Parassitarie e Immunomediate, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161 Roma, Italy. E-mail: roberto.nisini{at}iss.it

The functional consequences of treating human monocytes with purified and chemically characterized Candida albicans β-glucan—a major microbial pathogen associated molecular pattern—on their differentiation into dendritic cells (DC) were investigated. We show here that β-glucan-treated monocytes differentiated into mature DC (Glu-MoDC) with altered phenotype and functional behavior, similarly to DC derived from C. albicans 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 β-glucan is a mixture of both β-(1,3) and β-(1,6) glucan, we investigated their relative contribution by the use of non-Candida β-glucan structural analogs. We found that high molecular weight (MW) glucans β–(1,6) pustulan and β-(1,3) curdlan totally mimicked the effect of C. albicans β-glucan, while the low MW β-(1,3) glucan laminarin did not have any effect. Because β-glucan is a common constituent of all fungi and is abundantly released in vivo during systemic fungal infection, this novel effect of β-glucan has potential implications for host-parasite relationship in candidiasis and other mycoses. In particular, our data suggest that β-glucan could bias noninfected, bystander monocytes, thus aggravating the general immunodeficiency, predisposing to systemic fungal infection.

Key Words: fungi • antigen presentation/processing • β-glucan structure






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