Abstract

Paracoccidioidomycosis (PCM) is the most relevant systemic endemic mycosis limited to Latin American countries. The etiological agents are thermally dimorphic species of the genus Paracoccidioides. Infection occurs via respiratory tract by inhalation of propagules from the environmental (saprophytic) phase. In the lung alveoli the fungus converts to the characteristic yeast phase (parasitic) where interact with extracellular matrix proteins, epithelial cells, and the host cellular immunity. The response involves phagocytic cells recognition but intracellular Paracoccidioides have demonstrated the ability to survive and also multiply inside the neutrophils, macrophages, giant cells, and dendritic cells. Persistence of Paracoccidioides as facultative intracellular pathogen is important in terms of the fungal load but also regarding to the possibility to disseminate penetrating other tissues even protected by the phagocytes. This strategy to invade other organs via transmigration of infected phagocytes is called Trojan horse mechanism and it was also described for other fungi and considered a factor of pathogenicity. This mini review comprises a literature revision of the spectrum of tools and mechanisms displayed by Paracoccidioides to overcame phagocytosis, discusses the Trojan horse model and the immunological context in proven models or the possibility that Paracoccidioides apply this tool for dissemination to other tissues.

Highlights

  • Onygenalean (Ascomycota) organisms including Paracoccidioides, have typically adapted to saprobic conditions in soil and to the live tissues of animal hosts

  • The dimorphic transition to the yeast form and the interaction with the extracellular matrix (ECM) proteins, epithelial cells, and the host cellular immunity mediated by the phagocytic cells of the innate immune and adaptive systems, they are the first steps in a complex relationship between Paracoccidioides and the host that can lead to a granulomatous disease

  • Due to the capability of human Polymorphonuclear neutrophils (PMNs) to release higher oxygen metabolites, an activation process by interferon gamma (IFN-g), TNF-a, and GM-CSF cytokines is required for killing P. brasiliensis (Rodrigues et al, 2007)

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Summary

Gustavo Giusiano*

Mycology Department, Instituto de Medicina Regional, Universidad Nacional del Nordeste, Consejo Nacional de Investigaciones Científicas y Tecnicas (CONICET), Resistencia, Argentina. Persistence of Paracoccidioides as facultative intracellular pathogen is important in terms of the fungal load and regarding to the possibility to disseminate penetrating other tissues even protected by the phagocytes. This strategy to invade other organs via transmigration of infected phagocytes is called Trojan horse mechanism and it was described for other fungi and considered a factor of pathogenicity. This mini review comprises a literature revision of the spectrum of tools and mechanisms displayed by Paracoccidioides to overcame phagocytosis, discusses the Trojan horse model and the immunological context in proven models or the possibility that Paracoccidioides apply this tool for dissemination to other tissues

INTRODUCTION
The Trojan Horse Model in Paracoccidioides
Phagocytes Activation
How to Survive and Even Multiply Into the Phagocytes
Polymorphonuclear Neutrophils
Dendritic Cells
Spread via Transmigration of Infected Phagocytes
DISCUSSION
Full Text
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