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Candida albicans β-glucan exposure is controlled by the fungal CEK1-mediated mitogen-activated protein kinase pathway that modulates immune responses triggered through dectin-1

AutorGalán-Díez, Marta; Arana, David M.; Serrano-Gómez, Diego; Kremer, Leonor; Casasnovas, José María; Ortega, Mara; Cuesta-Domínguez, Álvaro; Corbí, Angel L. ; Pla, Jesús ; Fernández-Ruiz, Elena
Fecha de publicación2010
EditorAmerican Society for Microbiology
CitaciónInfection and Immunity 78(4) : 1426- 1436 (2010)
ResumenInnate immunity to Candida albicans depends upon the recognition of molecular patterns on the fungal cell wall. However, the masking of major components such as β-glucan seems to be a mechanism that fungi have evolved to avoid immune cell recognition through the dectin-1 receptor. Although the role of C. albicans mitogen-activated protein kinase (MAPK) pathways as virulence determinants has been established previously with animal models, the mechanism involved in this behavior is largely unknown. In this study we demonstrate that a disruption of the C. albicans extracellular signal-regulated kinase (ERK)-like 1 (CEK1)-mediated MAPK pathway causes enhanced cell wall β-glucan exposure, triggering immune responses more efficiently than the wild type, as measured by dectin-1-mediated specific binding and human dendritic cell (hDC)- and macrophage-mediated phagocytosis, killing, and activation of intracellular signaling pathways. At the molecular level, the disruption of CEK1 resulted in altered spleen tyrosine kinase (Syk), Raf-1, and ERK1/2 activations together with IκB degradation on hDCs and increased dectin-1-dependent activator protein 1 (AP-1) activation on transfected cells. In addition, concurring with these altered pathways, we detected increased reactive oxygen species production and cytokine secretion. In conclusion, the CEK1-mediated MAPK pathway is involved in β-glucan exposure in a fungal pathogen, hence influencing dectin-1-dependent immune cell recognition, thus establishing this fungal intracellular signaling route as a promising novel therapeutic target.
URIhttp://hdl.handle.net/10261/82243
DOI10.1128/IAI.00989-09
Identificadoresdoi: 10.1128/IAI.00989-09
issn: 0019-9567
e-issn: 1098-5522
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