Cell intrinsic galectin-3 attenuates neutrophil ROS-dependent killing of Candida by modulating CR3 downstream syk activation
Journal
Frontiers in Immunology
Journal Volume
8
Journal Issue
FEB
Pages
48
Date Issued
2017
Author(s)
Wu, Sheng-Yang
Huang, Juin-Hua
Chen, Wen-Yu
Chan, Yi-Chen
CHUN HUNG LIN
Liu, Fu-Tong
Abstract
cells. While galectin-3 deficiency modulates neutrophil and macrophage activation and the recruitment of monocytes and dendritic cells, the deficiency does not affect the numbers of infiltrating neutrophils or macrophages. Galectin-3 deficiency ameliorates systemic candidiasis by reducing fungal burden, renal pathology, and mortality. Adoptive transfer experiments demonstrate that cell intrinsic galectin-3 negatively regulates neutrophil effector functions against candidiasis. Reducing galectin-3 expression or activity by siRNA or gal3 inhibitor TD139 enhances human neutrophil ROS production. Mice treated with TD139 have enhanced ability to clear the fungus. Our work unravels the mechanism by which galectin-3 regulates Syk-dependent neutrophil fungicidal functions and raises the possibility that blocking gal3 in neutrophils may be a promising therapeutic strategy for treating systemic candidiasis.
SDGs
Publisher
Frontiers Research Foundation
Type
journal article