An Intracellular Arrangement of Histoplasma capsulatum Yeast-Aggregates Generates Nuclear Damage to the Cultured Murine Alveolar Macrophages

Frontiers in Microbiology
N S PitanguiA M Fusco-Almeida

Abstract

Histoplasma capsulatum is responsible for a human systemic mycosis that primarily affects lung tissue. Macrophages are the major effector cells in humans that respond to the fungus, and the development of respiratory disease depends on the ability of Histoplasma yeast cells to survive and replicate within alveolar macrophages. Therefore, the interaction between macrophages and H. capsulatum is a decisive step in the yeast dissemination into host tissues. Although the role played by components of cell-mediated immunity in the host's defense system and the mechanisms used by the pathogen to evade the host immune response are well understood, knowledge regarding the effects induced by H. capsulatum in host cells at the nuclear level is limited. According to the present findings, H. capsulatum yeast cells display a unique architectural arrangement during the intracellular infection of cultured murine alveolar macrophages, characterized as a formation of aggregates that seem to surround the host cell nucleus, resembling a "crown." This extranuclear organization of yeast-aggregates generates damage on the nucleus of the host cell, producing DNA fragmentation and inducing apoptosis, even though the yeast cells are not located inside t...Continue Reading

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Citations

Nov 30, 2016·Frontiers in Cellular and Infection Microbiology·Caroline M MarcosAna M Fusco-Almeida
Aug 6, 2020·Frontiers in Microbiology·Larissa Naiara Carvalho GonçalvesAna Marisa Fusco-Almeida

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Methods Mentioned

BETA
fluorescence microscopy
flow cytometry
electrophoresis
light microscopy
Confocal Microscopy
confocal scanning microscopy

Software Mentioned

IN Cell 1000 Workstation
TriTek CometScore
FACSDiva
IN Cell Analyzer
Investigator IN Cell 1000 Workstation
Investigator
BD

Related Concepts

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis