Event Abstract Back to Event C. albicans phagocytosis by mast cells via Toll like receptor-2: protection or immune escape? Karen H. Pinke1*, Heliton G. Lima1, Fernando Q. Cunha2 and Vanessa S. Lara1 1 Bauru School of Dentistry. University of São Paulo., Department of Stomatology, area of Pathology, Brazil 2 Faculty of Medicine of Ribeirão Preto. University of São Paulo., Department of Pharmacology., Brazil Candida albicans (C. albicans) is a fungus commonly found in the mucosa of the gastrointestinal tract, including the mouth, and may causecandidiasis, especially in immunosuppression. Mast cells reside in the subepithelial region and actively participate in innate immunity, like one of the first lines of defense against C. albicans. The recognition of this fungus can occur via different receptors, e.g. Toll-like receptor 2 (TLR2), present on the surface of mast cells. Thus, this study evaluated in vitro the relationship of the phagocytosis, intracellular oxide nitric production by mast cells challenged with C. albicans and the involvement of TLR2 in these mechanisms. For this, Murine bone marrow cells (BMMC) wild type (TLR2+ /+) or knockout (TLR2-/-) were cultured in presence of stem cell factor and interleukin-3. After, the BMMCs were challenged with FITC-labeled C. albicans by 60 minutes and the phagocytosis analyzed by confocal laser scanning microscopy. Furthermore, intracellular nitric oxide production was measured used the DAF-FM diacetate and spectrophotometer. Our results showed that BMMC TLR2+ /+ phagocytose C. albicans but did not showed overproduction of the nitric oxide after stimulation with fungus, in relation with the basal production. However, in the absence of the TLR2, the nitric oxide production is increased, while the phagocytosis is reduced, in comparison with wild mouse. Therefore, we conclude that the C. albicans recognition by TLR2 results in the increased phagocytosis, but without nitric oxide stimulous. This can represent an escape way of the fungus of the defense mechanisms developed by mast cells via TLR2. Keywords: Mast Cells, immune escape, Candida albicans, TLR2 signaling, Nitric Oxide Conference: 15th International Congress of Immunology (ICI), Milan, Italy, 22 Aug - 27 Aug, 2013. Presentation Type: Abstract Topic: Innate immunity Citation: Pinke KH, Lima HG, Cunha FQ and Lara VS (2013). C. albicans phagocytosis by mast cells via Toll like receptor-2: protection or immune escape?. Front. Immunol. Conference Abstract: 15th International Congress of Immunology (ICI). doi: 10.3389/conf.fimmu.2013.02.00054 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 08 Mar 2013; Published Online: 22 Aug 2013. * Correspondence: Mrs. Karen H Pinke, Bauru School of Dentistry. University of São Paulo., Department of Stomatology, area of Pathology, Bauru, Brazil, karen.pinke@gmail.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Karen H Pinke Heliton G Lima Fernando Q Cunha Vanessa S Lara Google Karen H Pinke Heliton G Lima Fernando Q Cunha Vanessa S Lara Google Scholar Karen H Pinke Heliton G Lima Fernando Q Cunha Vanessa S Lara PubMed Karen H Pinke Heliton G Lima Fernando Q Cunha Vanessa S Lara Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.