Stress Response in
            <i>Candida Glabrata</i>
            : Pieces of a Fragmented Picture

Jandric, Zeljkica; Schüller, Christoph

doi:10.2217/fmb.11.131

Cited by 19 publications

(12 citation statements)

References 83 publications

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“…Several lines of evidence suggest that these cells are of outstanding importance in the response against invasive Candida infections. PMN govern the transcriptional response of C. albicans to incubation in human blood (Fradin et al ., ) and induce various stress responses (Rubin‐Bejerano et al ., ; Enjalbert et al ., ; Jandric and Schuller, ; Fukuda et al ., ). Primary PMN confrontation assays have shown that PMN can differentiate between yeast and filamentous forms of C. albicans and PMN are the only host cell type known so far that can effectively inhibit filamentation of C. albicans after phagocytosis (Wozniok et al ., ).…”

Section: Discussionmentioning

confidence: 99%

Neutrophil activation byCandida glabratabut notCandida albicanspromotes fungal uptake by monocytes

et al. 2015

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SummaryCandida albicans and Candida glabrata account for the majority of candidiasis cases worldwide. Although both species are in the same genus, they differ in key virulence attributes. Within this work, live cell imaging was used to examine the dynamics of neutrophil activation after confrontation with either C. albicans or C. glabrata. Analyses revealed higher phagocytosis rates of C. albicans than C. glabrata that resulted in stronger PMN (polymorphonuclear cells) activation by C. albicans. Furthermore, we observed differences in the secretion of chemokines, indicating chemotactic differences in PMN signalling towards recruitment of further immune cells upon confrontation with Candida spp. Supernatants from co-incubations of neutrophils with C. glabrata primarily attracted monocytes and increased the phagocytosis of C. glabrata by monocytes. In contrast, PMN activation by C. albicans resulted in recruitment of more neutrophils. Two complex infection models confirmed distinct targeting of immune cell populations by the two Candida spp.: In a human whole blood infection model, C. glabrata was more effectively taken up by monocytes than C. albicans and histopathological analyses of murine model infections confirmed primarily monocytic infiltrates in C. glabrata kidney infection in contrast to PMN-dominated infiltrates in C. albicans infection. Taken together, our data demonstrate that the human opportunistic fungi C. albicans and C. glabrata are differentially recognized by neutrophils and one outcome of this differential recognition is the preferential uptake of C. glabrata by monocytes.

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Section: Discussionmentioning

confidence: 99%

Neutrophil activation byCandida glabratabut notCandida albicanspromotes fungal uptake by monocytes

et al. 2015

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“…Its genome (ATCC 2001) covers 67 genes encoding putative adhesin-like GPI-modified cell wall proteins, including the Epa family with 17 members [59], and their expression is regulated. Moreover, C. glabrata cells carrying mutations in some loci show a rise in adherence to epithelial cells and are able to colonize organs more efficiently [60][61][62]. In fact, there are several factors tangled in the development of C. glabrata infection.…”

Section: Candida Glabrata-host Interactionsmentioning

confidence: 99%

Candida glabrata: a review of its features and resistance

Rodrigues

Silva

Henriques

2013

Eur J Clin Microbiol Infect Dis

243

258

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Candida species belong to the normal microbiota of the oral cavity and gastrointestinal and vaginal tracts, and are responsible for several clinical manifestations, from mucocutaneous overgrowth to bloodstream infections. Once believed to be non-pathogenic, Candida glabrata was rapidly blamable for many human diseases. Year after year, these pathological circumstances are more recurrent and problematic to treat, especially when patients reveal any level of immunosuppression. These difficulties arise from the capacity of C. glabrata to form biofilms and also from its high resistance to traditional antifungal therapies. Thus, this review intends to present an excerpt of the biology, epidemiology, and pathology of C. glabrata, and detail an approach to its resistance mechanisms based on studies carried out up to the present.

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“…Notably, both loci encode identical histone H3 and H4 proteins [20], and one H3-H4 gene locus is required for cell viability [21]. Owing to the phylogenetic relatedness between C. glabrata and S. cerevisiae, chromatin organization, DNA damage repair and stress response mechanisms are presumed to be similar between these two yeasts [22][23][24].…”

Section: Introductionmentioning

confidence: 99%

Histone H4 dosage modulates DNA damage response in the pathogenic yeast Candida glabrata via homologous recombination pathway

2020

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Candida glabrata, a nosocomial fungal bloodstream pathogen, causes significant morbidity and mortality in hospitals worldwide. The ability to replicate in macrophages and survive a high level of oxidative stress contributes to its virulence in the mammalian host. However, the role of DNA repair and recombination mechanisms in its pathobiology is still being discovered. Here, we have characterized the response of C. glabrata to the methyl methanesulfonate (MMS)-induced DNA damage. We found that the MMS exposure triggered a significant downregulation of histone H4 transcript and protein levels, and that, the damaged DNA was repaired by the homologous recombination (HR) pathway. Consistently, the reduced H4 gene dosage was associated with increased HR frequency and elevated resistance to MMS. The genetic analysis found CgRad52, a DNA strand exchange-promoter protein of the HR system, to be essential for this MMS resistance. Further, the tandem-affinity purification and mass spectrometry analysis revealed a substantially smaller interactome of H4 in MMS-treated cells. Among 23 identified proteins, we found the WD40-repeat protein CgCmr1 to interact genetically and physically with H4, and regulate H4 levels, HR pathway and MMS stress survival. Controlling H4 levels tightly is therefore a regulatory mechanism to survive MMS stress in C. glabrata.

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Stress Response in Candida Glabrata : Pieces of a Fragmented Picture

Cited by 19 publications

References 83 publications

Neutrophil activation byCandida glabratabut notCandida albicanspromotes fungal uptake by monocytes

Neutrophil activation byCandida glabratabut notCandida albicanspromotes fungal uptake by monocytes

Candida glabrata: a review of its features and resistance

Histone H4 dosage modulates DNA damage response in the pathogenic yeast Candida glabrata via homologous recombination pathway

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