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Transcriptomic profiling of lung alveolar macrophages reveals distinct contribution of sterol metabolism in macrophage response to Cryptococcus gattii infection

ABSTRACT: Alveolar macrophages are key first responders to pulmonary cryptococcosis, but there is still limited knowledge on the dynamic molecular changes during Cryptococcus gattii infection. We therefore analyzed the transcriptional profiles of alveolar macrophages isolated from mice infected intranasally with C. gattii and compared those infected with C. neoformans or treated with PBS at 7 days postinfection, using RNA sequencing. In C. gattii-infected mice, alveolar macrophages displayed the alteration of gene expression linked to sterol biosynthesis, while macrophages from C. neoformans-infected mice were primarily associated with interferon and cytokine signaling pathways. Thus, our research revealed the distinct patterns in the alveolar macrophage response to C. gattii infection.

ORGANISM(S): Mus musculus

PROVIDER: GSE281113 | GEO | 2025/10/05

REPOSITORIES: GEO

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Project description:An array analysis of C. gattii (C. bacillosporus), intended to identify loci associated with the hypervirulence of the Vancouver Island Outbreak (VIO). 23 C. gattii isolates, representing both VIO strains and control strains, were grown for 24 hours in mammalian macrophages. RNA was isolated and gene expression for each strain quantified relative to pooled RNA from all 23 samples. Linear regression was used to identify loci showing positive or negative correlation with "intracellular proliferation rate", a proxy measure for virulence. Data from this analysis is included in Ma et al, 2009, PNAS 106(31) 12980-12985. The abstract is included below. In 1999, the population of Vancouver Island, Canada, began to experience an outbreak of a fatal fungal disease caused by a highly virulent lineage of Cryptococcus gattii. This organism has recently spread to the Canadian mainland and Pacific Northwest, but the molecular cause of the outbreak remains unknown. Here we show that the Vancouver Island outbreak (VIO) isolates have dramatically increased their ability to replicate within macrophages of the mammalian immune system in comparison with other C. gattii strains. We further demonstrate that such enhanced intracellular parasitism is directly linked to virulence in a murine model of cryptococcosis, suggesting that this phenotype may be the cause of the outbreak. Finally, microarray studies on 24 C. gattii strains reveals that the hypervirulence of the VIO isolates is characterized by the up-regulation of a large group of genes, many of which are encoded by mitochondrial genome or associated with mitochondrial activities. This expression profile correlates with an unusual mitochondrial morphology exhibited by the VIO strains after phagocytosis. Our data thus demonstrate that the intracellular parasitism of macrophages is a key driver of a human disease outbreak, a finding that has significant implications for a wide range of other human pathogens. Dual-colour hybridization (each sample was hybridized against pooled RNA), one array per isolate, 23 biological samples, no technical replicates.

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Transcriptomic profiling of lung alveolar macrophages reveals distinct contribution of sterol metabolism in macrophage response to Cryptococcus gattii infection

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