Role of phosphatidylinositol-3-kinase (PI3K), extracellular signal-regulated kinase (ERK) and nuclear transcription factor kappa beta (NF-k beta) on neutrophil phagocytic process of Candida albicans

Abstract

In humans, Candida albicans is the microorganism most frequently associated with fungal infections. Alterations in the balance between the host and this commensal pathogen, turns into a parasitic relationship which results in the development of invasive infections. Neutrophils via chemotaxis, phagocytosis, and microbicide capacity can eradicate this pathogen. Taken together, the aim of this work was to study the possible role of phosphatidylinositol-3-kinase (PI3K), extracellular signal-regulated kinase (ERK) and the nuclear transcription factor kappa beta (NF-k beta) on the phagocytic process of neutrophils. The chemotactic capacity of neutrophils and their ability to phagocytose and to destroy C. albicans in absence and presence of 1, 10, or 100 microM of wortmannin (a PI3K inhibitor); 10, 25, or 50 microM of Bay 11-7082 (a NF-k beta inhibitor) or 1, 5 or 10 microM of PD 98,059 (an ERK inhibitor) were determined. Our results show that fMLP-induced chemotaxis needs the participation of PI3K and NF-k beta. In contrast, ERK seems not to be involved. On the other hand, the inhibition of NF-kappa beta and ERK decreased neutrophil phagocytosis and microbicide capacity against C. albicans. However, both the phagocytic and candicide capacities were PI3K independent.