Taxonomic group: fungi / Basidiomycota
(Phylum: Basidiomycota)
NCBI PubMed ID: 23608320Publication DOI: 10.1016/j.fgb.2013.04.005Journal NLM ID: 9607601Publisher: Orlando, FL : Academic Press / Elsevier
Correspondence: Rodrigues ML <marciolr
cdts.fiocruz.br>
Institutions: Instituto de Microbiologia Professor Paulo de Góes, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil, Department of Microbiology and Immunology, Albert Einstein College of Medicine, New York, NY, USA, Departamento de Microbiologia, Imunologia e Parasitologia, Instituto Biomédico, Universidade Federal Fluminense, Brazil, Centro de Biotecnologia and Departamento de Biologia Molecular e Biotecnologia, Universidade Federal do Rio Grande do Sul, Brazil, Instituto de Ciências Biomédicas, Universidade de São Paulo, Brazil, Laboratório de Ultraestrutura Celular Hertha Meyer, Instituto de Biofisica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Brazil, f Laboratório de Biologia, Instituto Nacional de Metrologia, Normalização e Qualidade Industrial (INMETRO), Rio de Janeiro, Brazil, Division of Infectious Diseases of the Department of Medicine, Albert Einstein College of Medicine, New York, USA, i Fundação Oswaldo Cruz (Fiocruz), Centro de Desenvolvimento Tecnológico em Saúde (CDTS), Rio de Janeiro, Brazil
The principal capsular component of Cryptococcus neoformans, glucuronoxylomannan (GXM), interacts with surface glycans, including chitin-like oligomers. Although the role of GXM in cryptococcal infection has been well explored, there is no information on how chitooligomers affect fungal pathogenesis. In this study, surface chitooligomers of C. neoformans were blocked through the use of the wheat germ lectin (WGA) and the effects on animal pathogenesis, interaction with host cells, fungal growth and capsule formation were analyzed. Treatment of C. neoformans cells with WGA followed by infection of mice delayed mortality relative to animals infected with untreated fungal cells. This observation was associated with reduced brain colonization by lectin-treated cryptococci. Blocking chitooligomers also rendered yeast cells less efficient in their ability to associate with phagocytes. WGA did not affect fungal viability, but inhibited GXM release to the extracellular space and capsule formation. In WGA-treated yeast cells, genes that are involved in capsule formation and GXM traffic had their transcription levels decreased in comparison with untreated cells. Our results suggest that cellular pathways required for capsule formation and pathogenic mechanisms are affected by blocking chitin-derived structures at the cell surface of C. neoformans. Targeting chitooligomers with specific ligands may reveal new therapeutic alternatives to control cryptococcosis.
virulence, capsule, Cryptococcus neoformans, lectin binding, chitin oligosaccharides
Structure type: homopolymer ; n=3-20
Location inside paper: p. 65, column 1, paragraph 2
Trivial name: chitooligomer
Compound class: glucan
Contained glycoepitopes: IEDB_135813,IEDB_137340,IEDB_141807,IEDB_151531,IEDB_153212,IEDB_241099,IEDB_423114,IEDB_423150,SB_74,SB_85
Methods: PCR, biological assays, genetic methods, immunofluorescence analyses, fluorescence microscopy, flow cytometry, SEM, ANOVA
Biological activity: contribute to the pathogenesis of Cryptococcus neoformans, particulary participates in dissimination
Related record ID(s): 44855, 44856, 44877, 44889, 44899, 44913, 44915, 44916, 44917, 44925, 44940, 44941
NCBI Taxonomy refs (TaxIDs): 5207Reference(s) to other database(s): GTC:G97099AY
Show glycosyltransferases
There is only one chemically distinct structure:
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