Modulação da resposta de células epiteliais alveolar humanas tipo II infectadas com Cryptococcus neoformans com a presença do receptor FPR2/ALX

Abstract

The bronchial epithelium has defense mechanisms based on innate immunity against several airborne microorganisms including Cryptococcus neoformans. Formyl peptide receptor 2 (FPR2/ALX), a G protein-coupled receptor (GPCR), plays an important role in the inflammation and resolution processes, including in the airways. Here, we evaluated the inflammatory effects of C. neoformans using A549 epithelial cells, which do not express FPR2/ALX, and A549 transfected with full-length recombinant human FPR2/ALX (rhFPR2/ALX) cDNA. A549 cells with and without FPR2/ALX expression were exposed to C. neoformans (MOI 100) and analyzes were performed 24 hours after stimulation. C. neoformans increased IL-6 and IL-10 production (but not IL-8 and TGF-β1) and activated ERK1/2 and NF-kB phosphorylation in both cells with and without FPR2/ALX compared to controls. The adhesion and internalization of C. neoformans was not altered by the expression of FPR2/ALX. We concluded that the presence of the receptor FPR2/ALX was not capable of providing changes in inflammatory parameters in A549 cells infected with C. neoformans.