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Infection and Immunity, December 2005, p. 7860-7868, Vol. 73, No. 12
0019-9567/05/$08.00+0 doi:10.1128/IAI.73.12.7860-7868.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Instituto de Microbiologia Professor Paulo de Góes, Departamento de Microbiologia Geral, Universidade Federal do Rio de Janeiro, CCS, Bloco I, Ilha do Fundão, Rio de Janeiro, RJ, 21941-590,1 Disciplina de Biologia Celular, Universidade Federal de São Paulo, São Paulo, SP 04023-062,2 Centro de Biociências e Biotecnologia, Universidade Estadual do Norte Fluminense Darcy Ribeiro, Campos,3 Instituto de Biofísica Carlos Chagas Filho, Univesidade Federal do Rio de Janeiro, Rio de Janeiro,4 Departamento de Parasitologia, Universidade de São Paulo, São Paulo, SP, 05508-900,6 Departamento de Analises Clinicas e Toxicologicas, Universidade de São Paulo, SP, 05508-900, Brazil,7 Department of Biological Sciences, University of TexasEl Paso, El Paso, Texas 79968-05195
Received 3 August 2005/ Returned for modification 16 August 2005/ Accepted 29 August 2005
Monohexosylceramides (CMHs, or cerebrosides) have been reported as membrane and cell wall constituents of both pathogenic and nonpathogenic fungi, presenting remarkable differences in their ceramide moiety compared to mammalian CMHs. Current evidence suggests that CMHs are involved in fungal differentiation and growth and contribute to host immune response. Here we describe a structural diversity between cerebrosides obtained from different forms of the human pathogen Fonsecaea pedrosoi. The major CMH species produced by conidial forms displayed the same structure previously demonstrated by our group for mycelia, an N-2'-hydroxyhexadecanoyl-1-ß-D-glucopyranosyl-9-methyl-4,8-sphingadienine. However, the major cerebroside species purified from sclerotic cells carries an additional hydroxyl group, bound to its long-chain base. The structural difference between cerebrosides from mycelial and sclerotic cells was apparently not relevant for their antigenicity, since they were both recognized at similar levels by sera from individuals with chromoblastomycosis and a monoclonal antibody to a conserved cerebroside structure. Preincubation of fungal cells with anti-CMH monoclonal antibodies had no effect on the interaction of F. pedrosoi sclerotic cells with murine macrophages. In contrast to what has been described for other fungal species, sclerotic bodies are resistant to the antifungal action of anti-CMH antibodies. Immunofluorescence analysis showed that recognition of sclerotic cells by these antibodies only occurs at cell wall regions in which melanization is not evident. Accordingly, melanin removal with alkali results in an increased reaction of fungal cells with anti-CMH antibodies. Our results indicate that cerebroside expression in F. pedrosoi cells is associated with dimorphism and melanin assembly on the fungal cell wall.
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