IMBIV   05474
INSTITUTO MULTIDISCIPLINARIO DE BIOLOGIA VEGETAL
Unidad Ejecutora - UE
artículos
Título:
Oxidative and nitrosative stress responses during macrophage-Candida albicans biofilm interaction
Autor/es:
ARCE MIRANDA, JULIO E; PARAJE, M GABRIELA; BARONETTI, JOSÉ L; SOTOMAYOR, CLAUDIA E
Revista:
MEDICAL MYCOLOGY
Editorial:
TAYLOR & FRANCIS LTD
Referencias:
Lugar: Londres; Año: 2017
ISSN:
1369-3786
Resumen:
Candida albicans is an important source of device-associated infection because of its capacityfor biofilm formation. This yeast has the ability to form biofilms which favors thepersistence of the infection. Furthermore, the innate immune response has a critical rolein the control of these infections and macrophages (Mø) are vital to this process. An importantfungicidal mechanism employed by Mø involves the generation of toxic reactiveoxygen species (ROS) and reactive nitrogen intermediates (RNI). The interaction betweenbiofilms and these immune cells, and the contribution of oxidative and nitrosative stress,that is determinant to the course of the infection, remains elusive. The aim of this studywas to investigate this interaction. To this purpose, two models of Mø-biofilms contact,early (model 1) and mature (model 2) biofilms, were used; and the production of ROS,RNI and the oxidative stress response (OSR) were evaluated.We found that the presenceof Mø decreased the biofilm formation at an early stage and increased the productionof ROS and RNI, with activation of ORS (enzymatic and nonenzymatic). On the otherhand, the interaction between mature biofilms and Mø resulted in an increasing biofilmformation, with low levels of RNI and ROS production and decrease of OSR. Dynamicinteractions between Mø and fungal biofilms were also clearly evident from images obtainedby confocal scanning laser microscopy. The prooxidant-antioxidant balance wasdifferent depending of C. albicans biofilms stages and likely acts as a signal over theirformation in presence of Mø. These results may contribute to a better understanding ofthe immune-pathogenesis of C. albicans biofilm infections.