Enhanced proinflammatory response to the Candida albicans gpi7 null mutant by murine cells.

6533b831fe1ef96bd129901f

RESEARCH PRODUCT

Enhanced proinflammatory response to the Candida albicans gpi7 null mutant by murine cells.

Mathias L. Richard Celia Murciano Daniel Gozalbo Claude Gaillardin M. Luisa Gil Alberto Yáñez Armêl Plaine

subject

MESH: Inflammation Glycosylphosphatidylinositols Neutrophils medicine.medical_treatment Interleukin-1beta souris MESH: Neutrophils MESH: Virulence MESH: Mice Knockout Mice MESH: Interleukin-1beta Null cell MESH: Animals Candida albicans Peritoneal Cavity Cells Cultured Mice Knockout 0303 health sciences Toll-like receptor biology Virulence MESH: Toll-Like Receptor 2 MESH: Peritoneal Cavity MESH: Toll-Like Receptor 4 MESH: Glycosylphosphatidylinositols Infectious Diseases Cytokine MESH: Survival Analysis Tumor necrosis factor alpha MESH: Fungal Proteins protéine de la paroi cellulaire MESH: Macrophages Peritoneal MESH: Cells Cultured Virulence Factors Immunology Microbiology Microbiology Proinflammatory cytokine Fungal Proteins 03 medical and health sciences MESH: Mice Inbred C57BL medicine Animals MESH: Mice 030304 developmental biology MESH: Virulence Factors Inflammation 030306 microbiology Interleukin-6 Tumor Necrosis Factor-alpha MESH: Candida albicans [SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biology biology.organism_classification Survival Analysis pathogénicité MESH: Interleukin-6 Toll-Like Receptor 2 Mice Inbred C57BL Toll-Like Receptor 4 TLR2 Glycosylphosphatidylinositol MESH: Gene Deletion MESH: Tumor Necrosis Factor-alpha TLR4 Macrophages Peritoneal candida albicans immunité Gene Deletion

description

International audience; The Candida albicans gpi7/gpi7 null mutant strain (Deltagpi7), which is affected in glycosylphosphatidylinositol (GPI) anchor biosynthesis, showed a reduced virulence following systemic infection of C57BL/6 mice. In vitro production of TNF-alpha, IL-6 and IL-1beta by macrophages in response to Deltagpi7 cells was significantly increased as compared to control (wild type GPI7/GPI7 and revertant gpi7/GPI7) cells; this probably contributes to the enhanced recruitment of neutrophils to the peritoneal cavity in response to Deltagpi7 cells. Survival of knockout mice for Toll-like receptor (TLR) 2 and TLR4 following intravenous injection of Deltagpi7 cells showed no significant differences as compared to C57BL/6 mice. In vitro production of TNF-alpha by macrophages and neutrophil recruitment were significantly inhibited in TLR2-/- mice in response to control yeast strains. Interestingly both TNF-alpha production and neutrophil recruitment in response to Deltagpi7 were significantly increased in all three types of mice, with no differences among them, and laminarin failed to inhibit this increased production of TNF-alpha. These results indicate that the enhanced proinflammatory response to Deltagpi7 does not involve recognition through TLR2, TLR4 nor dectin-1. Therefore, complete GPI anchors confer surface properties that are involved in modulation of cytokine production by macrophages in response to C. albicans.

year	journal	country	edition	language
2008-04-01

10.1016/j.micinf.2007.12.018 https://hal.archives-ouvertes.fr/hal-00315487