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CRYPTOCOCCUS NEOFORMANS RELEASES PROTEINS DURING INTRACELLULAR RESIDENCE THAT AFFECT THE OUTCOME OF THE FUNGAL–MACROPHAGE INTERACTION
Proteínas Fúngicas
Vesículas Extracelulares
Macrófagos
Fatores de Virulência
Author
Affilliation
Department of Molecular Microbiology and Immunology. Johns Hopkins School of Public Health. Baltimore, United States.
Laboratory of Clinical Immunology and Microbiology. National Institute of Allergy and Infectious Disease. National Institutes of Health. Memorial Drive. Bethesda, United States.
Department of Molecular Microbiology and Immunology. Johns Hopkins School of Public Health. Baltimore, United States.
Department of Molecular and Cell Biology. Johns Hopkins University. Baltimore, United States.
Department of Molecular Microbiology and Immunology. Johns Hopkins School of Public Health. Baltimore, United States.
Fundação Oswaldo Cruz. Instituto Carlos Chagas. Curitiba, PR, Brasil. / Fundação Oswaldo Cruz. Centro de Desenvolvimento Tecnológico em Saúde. Rio de Janeiro, RJ, Brasil.
Department of Molecular Microbiology and Immunology. Johns Hopkins School of Public Health. Baltimore, United States.
Fundação Oswaldo Cruz. Instituto Carlos Chagas. Curitiba, PR, Brasil. / Universidade Federal do Rio de Janeiro. Instituto de Microbiologia Paulo de Góes. Rio de Janeiro, RJ, Brasil.
Department of Molecular Microbiology and Immunology. Johns Hopkins School of Public Health. Baltimore, United States.
Laboratory of Clinical Immunology and Microbiology. National Institute of Allergy and Infectious Disease. National Institutes of Health. Memorial Drive. Bethesda, United States.
Department of Molecular Microbiology and Immunology. Johns Hopkins School of Public Health. Baltimore, United States.
Department of Molecular Microbiology and Immunology. Johns Hopkins School of Public Health. Baltimore, United States.
MRC Centre for Medical Mycology. College of Health and Medicine. University of Exeter. Devon, United Kingdom.
Laboratory of Clinical Immunology and Microbiology. National Institute of Allergy and Infectious Disease. National Institutes of Health. Memorial Drive. Bethesda, United States.
Department of Molecular Microbiology and Immunology. Johns Hopkins School of Public Health. Baltimore, United States.
Department of Molecular and Cell Biology. Johns Hopkins University. Baltimore, United States.
Department of Molecular Microbiology and Immunology. Johns Hopkins School of Public Health. Baltimore, United States.
Fundação Oswaldo Cruz. Instituto Carlos Chagas. Curitiba, PR, Brasil. / Fundação Oswaldo Cruz. Centro de Desenvolvimento Tecnológico em Saúde. Rio de Janeiro, RJ, Brasil.
Department of Molecular Microbiology and Immunology. Johns Hopkins School of Public Health. Baltimore, United States.
Fundação Oswaldo Cruz. Instituto Carlos Chagas. Curitiba, PR, Brasil. / Universidade Federal do Rio de Janeiro. Instituto de Microbiologia Paulo de Góes. Rio de Janeiro, RJ, Brasil.
Department of Molecular Microbiology and Immunology. Johns Hopkins School of Public Health. Baltimore, United States.
Laboratory of Clinical Immunology and Microbiology. National Institute of Allergy and Infectious Disease. National Institutes of Health. Memorial Drive. Bethesda, United States.
Department of Molecular Microbiology and Immunology. Johns Hopkins School of Public Health. Baltimore, United States.
Department of Molecular Microbiology and Immunology. Johns Hopkins School of Public Health. Baltimore, United States.
MRC Centre for Medical Mycology. College of Health and Medicine. University of Exeter. Devon, United Kingdom.
Abstract
Cryptococcus neoformans is a facultative intracellular pathogen that can replicate and disseminate in mammalian macrophages. In this study, we analyzed fungal proteins identified in murine macrophage-like cells after infection with C. neoformans. To accomplish this, we developed a protocol to identify proteins released from cryptococcal cells inside macrophage-like cells; we identified 127 proteins of fungal origin in infected macrophage-like cells. Among the proteins identified was urease, a known virulence factor, and others such as transaldolase and phospholipase D, which have catalytic activities that could contribute to virulence. This method provides a straightforward methodology to study host–pathogen interactions. We chose to study further Yeast Oligomycin Resistance (Yor1), a relatively uncharacterized protein belonging to the large family of ATP binding cassette transporter (ABC transporters). These transporters belong to a large and ancient protein family found in all extant phyla.While ABC transporters have an enormous diversity of functions across varied species, in pathogenic fungi they are better studied as drug efflux pumps. Analysis of C. neoformans yor1 strains revealed defects in nonlytic exocytosis, capsule size, and dimensions of extracellular vesicles, when compared to wild-type strains. We detected no difference in growth rates and cell body size. Our results indicate that C. neoformans releases a large suite of proteins during macrophage infection, some of which can modulate fungal virulence and are likely to affect the fungal–macrophage interaction.
DeCS
Cryptococcus neoformansProteínas Fúngicas
Vesículas Extracelulares
Macrófagos
Fatores de Virulência
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