title: Candida albicans up-regulates the Fas-L expression in liver Natural Killer and Natural Killer T cells.
abstract: After Candida albicans arrival to the liver, the local production of proinflammatory cytokines and the expanded intrahepatic lymphocytes (IHL) can be either beneficial or detrimental to the host. Herein we explored the balance between protective inflammatory reaction and liver damage, focusing our study on the contribution of TNF-α and Fas-Fas-L pathways in the hepatocellular apoptosis associated to C. albicans infection. A robust tissue reaction and a progressive increase of IL-1β, IL-6 and TNF-α were observed in infected animals. Blocking the biological activity of TNF-α did not modify the number of apoptotic cells observed in C. albicans infected animals. Fas-L molecule was up regulated on purified hepatic mononuclear cells and its expression progressed with the infection. In the IHL compartment, the absolute number of Fas-L+ NK and NKT cells increased on days 1 and 3 of the infection. C. albicans was also able to up regulate Fas-L expression in normal liver NK and NKT cells after in vitro contact. The innate receptor TLR2 was involved in this phenomenon. In the interplay between host factors and evasion strategies exploited by pathogens, the mechanism supported here could represent an additional way that allows this fungus to circumvent protective immune responses in the liver.
authors.affiliation: Inmunología, Departamento de Bioquímica Clínica, Centro de Investigaciones en Bioquímica Clínica e Inmunología CIBICI-CONICET, Facultad de Ciencias Químicas. Universidad Nacional de Córdoba, Córdoba, Argentina.
authors.forename: María Sol
authors.initials: MS
authors.lastname: Renna
authors.affiliation: Inmunología, Departamento de Bioquímica Clínica, Centro de Investigaciones en Bioquímica Clínica e Inmunología CIBICI-CONICET, Facultad de Ciencias Químicas. Universidad Nacional de Córdoba, Córdoba, Argentina.
authors.forename: Carlos Mauricio
authors.initials: CM
authors.lastname: Figueredo
authors.affiliation: Inmunología, Departamento de Bioquímica Clínica, Centro de Investigaciones en Bioquímica Clínica e Inmunología CIBICI-CONICET, Facultad de Ciencias Químicas. Universidad Nacional de Córdoba, Córdoba, Argentina.
authors.forename: María Cecilia
authors.initials: MC
authors.lastname: Rodríguez-Galán
authors.affiliation: Inmunología, Departamento de Bioquímica Clínica, Centro de Investigaciones en Bioquímica Clínica e Inmunología CIBICI-CONICET, Facultad de Ciencias Químicas. Universidad Nacional de Córdoba, Córdoba, Argentina.
authors.forename: Paula Alejandra
authors.initials: PA
authors.lastname: Icely
authors.affiliation: Inmunología, Departamento de Bioquímica Clínica, Centro de Investigaciones en Bioquímica Clínica e Inmunología CIBICI-CONICET, Facultad de Ciencias Químicas. Universidad Nacional de Córdoba, Córdoba, Argentina.
authors.forename: Hugo
authors.initials: H
authors.lastname: Cejas
authors.affiliation: Inmunología, Departamento de Bioquímica Clínica, Centro de Investigaciones en Bioquímica Clínica e Inmunología CIBICI-CONICET, Facultad de Ciencias Químicas. Universidad Nacional de Córdoba, Córdoba, Argentina.
authors.forename: Roxana
authors.initials: R
authors.lastname: Cano
authors.affiliation: Inmunología, Departamento de Bioquímica Clínica, Centro de Investigaciones en Bioquímica Clínica e Inmunología CIBICI-CONICET, Facultad de Ciencias Químicas. Universidad Nacional de Córdoba, Córdoba, Argentina.
authors.forename: Silvia Graciela
authors.initials: SG
authors.lastname: Correa
authors.affiliation: Inmunología, Departamento de Bioquímica Clínica, Centro de Investigaciones en Bioquímica Clínica e Inmunología CIBICI-CONICET, Facultad de Ciencias Químicas. Universidad Nacional de Córdoba, Córdoba, Argentina. Electronic address: csotomay@fcq.unc.edu.ar.
authors.forename: Claudia Elena
authors.initials: CE
authors.lastname: Sotomayor
mesh_terms: D000818:Animals; D017209:Apoptosis; D002176:Candida albicans / Q000276:immunology*; D018925:Chemokines / Q000235:genetics / Q000378:metabolism; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D053222:Fas Ligand Protein / Q000235:genetics*; D005260:Female; D005786:Gene Expression Regulation; D022781:Hepatocytes / Q000276:immunology; D007249:Inflammation / Q000276:immunology / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D007694:Killer Cells, Natural / Q000276:immunology* / Q000378:metabolism*; D008099:Liver / Q000276:immunology / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D055611:Natural Killer T-Cells / Q000276:immunology* / Q000378:metabolism*; D051381:Rats; D015398:Signal Transduction; D051195:Toll-Like Receptor 2 / Q000235:genetics / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D018925:Chemokines; D016207:Cytokines; D053222:Fas Ligand Protein; D051195:Toll-Like Receptor 2; D014409:Tumor Necrosis Factor-alpha
keywords: Candida albicans; Fas-Fas-L; Liver NK cells; Liver NKT cells; TLR2; TNF-alpha