Phagocytosis of Candida Albicans Induces Apoptosis of Human Neutrophils

Rotstein, Dalia; Parodo, Jean; Taneja, Ravi; Marshall, John C.

doi:10.1097/00024382-200014030-00006

Cited by 60 publications

(53 citation statements)

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“…Depending on their parasitic behavior, differential triggering of cell survival or cell death is used by microbes to promote their survival. The yeast C. albicans has been reported to inhibit tumor necrosis factor-␣-induced DNA fragmentation in macrophages (33) and to induce apoptosis of macrophages (24) and neutrophils (25), but the mechanisms and C. albicans molecules involved are unknown. It has previously been shown that, in contrast to the nonpathogenic yeast S. cerevisiae, C. albicans was able to specifically alter signal transduction of the MEK-ERK pathway (3).…”

Section: Discussionmentioning

confidence: 99%

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Candida albicans Phospholipomannan Promotes Survival of Phagocytosed Yeasts through Modulation of Bad Phosphorylation and Macrophage Apoptosis

Ibata-Ombetta

Idziorek

Trinel

et al. 2003

Journal of Biological Chemistry

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The surface of the pathogenic yeast Candida albicans is coated with phospholipomannan (PLM), a phylogenetically unique glycolipid composed of ␤-1,2-oligomannosides and phytoceramide. This study compared the specific contribution of PLM to the modulation of signaling pathways linked to the survival of C. albicans in macrophages in contrast to Saccharomyces cerevisiae. C. albicans endocytosis by J774 and disregulation of the ERK1/2 signal transduction pathway was associated downstream with a reduction in Bad Ser-112 phosphorylation and disappearance of free Bcl-2. This suggested an apoptotic effect, which was confirmed by staining of phosphatidylserine in the macrophage outer membrane. The addition of PLM to macrophages incubated with S. cerevisiae mimicked each of the disregulation steps observed with C. albicans and promoted the survival of S. cerevisiae. Externalization of membranous phosphatidylserine, loss of mitochondrial integrity, and DNA fragmentation induced by PLM showed that this molecule promoted yeast survival by inducing host cell death. These findings suggest strongly that PLM is a virulence attribute of C. albicans and that elucidation of the relationship between structure and apoptotic activity is an innovative field of research.

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Section: Discussionmentioning

confidence: 99%

“…In host tissues, C. albicans may be both intra-and extracellular (23). Macrophages undergo apoptotic cell death after infection with C. albicans strains capable of hyphal formation (24), and activation of caspase 3 has been observed after endocytosis of C. albicans by neutrophils (25).…”

mentioning

confidence: 99%

Candida albicans Phospholipomannan Promotes Survival of Phagocytosed Yeasts through Modulation of Bad Phosphorylation and Macrophage Apoptosis

Ibata-Ombetta

Idziorek

Trinel

et al. 2003

Journal of Biological Chemistry

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“…[8][9][10][11] Conversely, this delayed apoptosis can be counterbalanced by others mediators such as TNF-a, IL-10, activation of oxidative burst, or phagocytosis of some bacterial species. 4,[12][13][14][15][16] The transmigration process is initiated by the activation of neutrophils stimulated by inflammatory agents. Then, PMN migration requires sequential engagement of PMN adhesion molecules to their counter receptors on the endothelium, within the extracellular matrix and finally, on the epithelium.…”

Section: Introductionmentioning

confidence: 99%

Downregulation of caspases and Fas ligand expression, and increased lifespan of neutrophils after transmigration across intestinal epithelium

et al. 2003

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During inflammatory bowel diseases, commitment of extravased polymorphonuclear leucocytes (PMN) to apoptosis is required for the resolution of inflammation. To investigate the effect of transepithelial migration on PMN apoptotic rates, PMN transepithelial migration was reproduced in vitro using T84 intestinal monolayers. Transepithelial migration was found to delay neutrophil apoptosis, and this survival effect correlated with a downregulation of the surface expression of Fas ligand (FasL) and with a decrease in both procaspases-3, and -8 mRNA and procaspases-3, -6, -7 and -8 protein levels. Moreover, neutrophil survival and FasL shedding mediated by transepithelial migration were abrogated by a broad-spectrum metalloproteinase inhibitor, BB-94. Although Erk1/2 and p38 MAPK were activated in transmigrated PMN, inhibition of these MAP kinases did not impair transmigration-induced PMN survival. Taken together, our results show that transepithelial migration induces the downregulation of proapoptotic proteins expression in transmigrated PMN, which results in their increased lifespan.

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“…Phagocytosis of heat-killed C. albicans increased the apoptosis of human neutrophils after culture for 18 h [14]. In contrast, infection by C. albicans inhibited apoptosis of human monocytes and supernates from co-cultures of neutrophils and C. albicans inhibited apoptosis of naive neutrophils [14][15][16].…”

Section: Introductionmentioning

confidence: 93%

Early membrane exposure of phosphatidylserine followed by late necrosis in murine macrophages induced by Candida albicans from an HIV-infected individual

Panagio¹,

Felipe

Vidotto³

et al. 2002

Journal of Medical Microbiology

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Phagocytosis of Candida Albicans Induces Apoptosis of Human Neutrophils

Cited by 60 publications

References 0 publications

Candida albicans Phospholipomannan Promotes Survival of Phagocytosed Yeasts through Modulation of Bad Phosphorylation and Macrophage Apoptosis

Candida albicans Phospholipomannan Promotes Survival of Phagocytosed Yeasts through Modulation of Bad Phosphorylation and Macrophage Apoptosis

Downregulation of caspases and Fas ligand expression, and increased lifespan of neutrophils after transmigration across intestinal epithelium

Early membrane exposure of phosphatidylserine followed by late necrosis in murine macrophages induced by Candida albicans from an HIV-infected individual

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