6533b85ffe1ef96bd12c267f

RESEARCH PRODUCT

Toll-like receptor-2 is essential in murine defenses against Candida albicans infections

Didier FradeliziEva VillamónDaniel GozalboM. Luisa GilPatricia RoigJosé-enrique O'connor

subject

Chemokinemedicine.medical_treatmentPhagocytosisChemokine CXCL2ImmunologyHyphaeCell CountReceptors Cell SurfaceMicrobiologyMicrobiologyMicePhagocytosisIn vivoCandida albicansmedicineAnimalsMacrophageCandida albicansCells CulturedMice KnockoutToll-like receptorMembrane GlycoproteinsbiologyTumor Necrosis Factor-alphaToll-Like ReceptorsCandidiasisFlow Cytometrybiology.organism_classificationImmunity InnateToll-Like Receptor 2Corpus albicansMice Inbred C57BLDisease Models AnimalInfectious DiseasesCytokineMacrophages Peritonealbiology.proteinChemokinesReactive Oxygen Species

description

In this work, we studied the role of toll-like receptor-2 (TLR2) in murine defenses against Candida albicans. TLR2-deficient mice experimentally infected intraperitoneally (i.p.) or intravenously (i.v.) in vivo had very significant impaired survival compared with that of control mice. In vitro production of TNF-alpha and macrophage inhibitory protein-2 (MIP-2) by macrophages from TLR2-/- mice in response to yeasts and hyphae of C. albicans were significantly lower (80% and 40%, respectively; P <0.05) than production by macrophages from wild-type mice. This impaired production of TNF-alpha and MIP-2 probably contributed to the 41% decreased recruitment of neutrophils to the peritoneal cavity of i.p. infected TLR2-/- mice. In contrast, in vitro phagocytosis of yeasts and production of reactive oxygen intermediates (ROI) were not affected in macrophages from TLR2-/- animals. Our data indicate that TLR2 plays a major role in the response of macrophages to C. albicans, triggering cytokine and chemokine expression, and it is essential for in vivo protection against infection.

yearjournalcountryeditionlanguage
2004-01-24Microbes and Infection
https://doi.org/10.1016/j.micinf.2003.09.020