Abstract
Event Abstract Back to Event Involvment of Notch-TLR signaling in experimental paracoccidioidomycosis Lavínia D. Romera1* and Sandro R. Almeida1 1 University of São Paulo, Clinical and Toxicological Analyses, Brazil Introduction: Paracoccidioidomycosis is a systemic mycosis of deep nature and granulomatosis that preferentially affects the lung tissue caused by Paracoccidioides brasiliensis, a thermal dimorphic fungus. It interacts with macrophages, cells that play an important role in regulation of immune response. Recently it has been demonstrated the importance of Notch receptors in regulating the activity of macrophages. Given that Notch signaling may be involved in modulating macrophage function, we evaluated the ability of the fungus modulate the activation of this pathway. Methods and Results: J774 macrophages, pre-stimulated with LPS or not, were interacted with yeast fungus, followed by analysis of real-time-PCR, phagocytosis-index and ELISA. The transcriptional analysis of Notch1 revealed an increased level of transcription in 24 hours, while there is a reduction of its ligand Delta4. However, we found that the fungus alone is not able to induce transcription of NF-kB, but when we stimulated with LPS together inhibition of Notch pathway, an increased level of transcripts was observed, suggesting that this factor is activated in the absence of Notch. In the same context, we observed that phagocytosis of yeasts by macrophages became more efficient. It was possible to verify that the fungus has the ability to promote the production of IL-6 via TLR-Notch, making us assume that this cytokine is important to the establishment of the disease. We also observed that the increased level of IL-6 is associated with decrease of TNF-α. In resume ours results suggest that P.brasiliensis uses the Notch signaling pathway as an escape mechanism. Acknowledgements FAPESP for the finacial support Keywords: Notch, Paracoccidioidomycosis, TLRs (Toll-like receptors), Paracoccidioides brasiliensis, Macrophages Conference: 15th International Congress of Immunology (ICI), Milan, Italy, 22 Aug - 27 Aug, 2013. Presentation Type: Abstract Topic: Host-pathogen interactions Citation: Romera LD and Almeida SR (2013). Involvment of Notch-TLR signaling in experimental paracoccidioidomycosis. Front. Immunol. Conference Abstract: 15th International Congress of Immunology (ICI). doi: 10.3389/conf.fimmu.2013.02.00317 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: 14 Mar 2013; Published Online: 22 Aug 2013. * Correspondence: Ms. Lavínia D Romera, University of São Paulo, Clinical and Toxicological Analyses, São Paulo, Brazil, lavinia.romera@yahoo.com.br 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 Lavínia D Romera Sandro R Almeida Google Lavínia D Romera Sandro R Almeida Google Scholar Lavínia D Romera Sandro R Almeida PubMed Lavínia D Romera Sandro R Almeida 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.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.