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Role of Dectin-1 and NETs release by human neutrophils in the exracelular killing of Paracoccidioides brasiliensis

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Author(s):
Tatiana Fernanda Bachiega Pinelli
Total Authors: 1
Document type: Doctoral Thesis
Press: Botucatu. 2015-03-03.
Institution: Universidade Estadual Paulista (Unesp). Faculdade de Medicina. Botucatu
Defense date:
Advisor: Ângela Maria Victoriano de Campos Soares; Luciane Alarcão Dias Melício
Abstract

Paracoccidiodomycosis is a systemic mycosis caused by the dimorphic fungus Paracoccidioides brasiliensis, which is endemic in Latin America. Since phagocytic cells play an important role during innate immune response against this fungus, we have studied the relationship between human neutrophils (PMNs) and P. brasiliensis, focusing on the effector mechanisms of these cells. Neutrophils can destroy microrganisms using at least 3 distint mechanisms: phagocytosis followed by destruction in a phagolysossome, secretion of antimicrobial molecules, and the more recently identified netosis, involving the release of neutrophil extracellular traps ( NETs) that are constituted by chromatin associated with different granule proteins with antimicrobial activities. Here, we showed for the first time, that yeast cells from P. brasiliensis strain 18 are able to induce the release of NETs in vitro, by binding to dectin-1 receptor on human neutrophils. These structures were evidenced by scanning electron microscopy, and specific NETs compounds such as histone and elastase were shown by confocal microscopy. Fungi were ensnared by NETs, denotting the role of these structures in confining infection, avoiding dissemination. In addition, disruption of NETs by treatment of cocultures with DNAse increased the fungi survival, evidencing their killing capacity (AU)

FAPESP's process: 10/18957-1 - Neutrophil extracellular traps (NETs) participation on human neutrophil fungicidal activity against Paracoccidioides brasiliensis
Grantee:Tatiana Fernanda Bachiega Pinelli
Support Opportunities: Scholarships in Brazil - Doctorate