Artigo Acesso aberto Revisado por pares

Interferon-gamma production by human neutrophils upon challenge with Paracoccidioides brasiliensis

2013; Frontiers Media; Volume: 4; Linguagem: Inglês

10.3389/conf.fimmu.2013.02.00584

ISSN

1664-3224

Autores

Rodrigues Daniela, Fernandes Reginaldo, Balderramas Helanderson, Bachiega Tatiana, Calvi Sueli, Luciane Alarcão Dias‐Melicio, Marcimara Penitenti, Ikoma Maura, Soares �ngela,

Tópico(s)

Nail Diseases and Treatments

Resumo

Event Abstract Back to Event Interferon-gamma production by human neutrophils upon challenge with Paracoccidioides brasiliensis Daniela R. Rodrigues1*, Reginaldo K. Fernandes1, Helanderson A. Balderramas1, Tatiana F. Bachiega1, Sueli A. Calvi2, Luciane A. Dias-Melicio3, Marcimara Penitenti4, Maura R. Ikoma4 and Ângela M. Soares1* 1 Universidade Estadual Paulista Júlio de Mesquita Filho, Departamento de Microbiologia e Imunologia, Brazil 2 Universidade Estadual Paulista Júlio de Mesquita Filho, Doenças Tropicais - FMB, Brazil 3 Universidade Estadual Paulista Júlio de Mesquita Filho, Patologia - FMB, Brazil 4 Fundação Amaral Carvalho de Jaú, Laboratório de Citometria de Fluxo, Brazil Paracoccidiodomycosis is a systemic mycosis caused by the fungus Paracoccidioides brasiliensis (Pb), which is endemic in Latin America. The host innate immune response against the fungus has been well characterized and several studies have clearly shown the important role played by phagocytic cells. Our laboratory has studied the relationship between human neutrophils (PMNs) / Pb focusing the effector mechanisms of these cells against the fungus. However, in last years, studies have shown that in addition to their phagocytic and killer functions, PMNs can modulate and instruct the immune response, since these cells have been shown to produce and release several cytokines. Thus, we evaluated whether PMNs stimulated with P. brasiliensis can modulate the immune response to a Th1 phenotype through the production of IFN-gamma, as well as the role of pathogen recognition receptors (PRRs) as TLR2, TLR4 and Dectin-1 in this production. Furthermore, we asked whether activation of the cells with the cytokines IL-12, IL-15 and IL-18 could result in increased levels of this cytokine. Peripheral blood PMNs obtained from 20 healthy donors were nonactivated or activated with IL-12, IL-15 or IL-18 in different concentrations and challenged with P. brasiliensis strain 18 (Pb18) for 2h, 4h, 12h, 24h and 48h and evaluated for IFN-gamma production, by ELISA. In other experiments, PMNs were treated with monoclonal antibodies anti-TLR2, TLR4 and Dectin-1, challenged with P.brasiliensis and evaluated for IFN-gamma production. We found that P. brasiliensis induces human PMNs to produce IFN-gamma, probably by binding to TLR4 and Dectin-1 receptors expressed by these cells. Moreover, cytokine levels were significantly increased when cells were activated with each of the tested cytokines or a combination of two of them, being the association IL-12 plus IL-15 the most effective. The results support our hypothesis that during infection by P. brasiliensis, human PMNs via the production of IFN-gamma modulate the adaptive immune response to a Th1 response pattern. Acknowledgements Support: FAPESP 2010/17405-5. Keywords: human neutrophils, Interferon-gamma, Paracoccidioides brasiliensis, Cytokines, PRRs Conference: 15th International Congress of Immunology (ICI), Milan, Italy, 22 Aug - 27 Aug, 2013. Presentation Type: Abstract Topic: Host-pathogen interactions Citation: Rodrigues DR, Fernandes RK, Balderramas HA, Bachiega TF, Calvi SA, Dias-Melicio LA, Penitenti M, Ikoma MR and Soares ÂM (2013). Interferon-gamma production by human neutrophils upon challenge with Paracoccidioides brasiliensis. Front. Immunol. Conference Abstract: 15th International Congress of Immunology (ICI). doi: 10.3389/conf.fimmu.2013.02.00584 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: 25 Apr 2013; Published Online: 22 Aug 2013. * Correspondence: Miss. Daniela R Rodrigues, Universidade Estadual Paulista Júlio de Mesquita Filho, Departamento de Microbiologia e Imunologia, Botucatu, São Paulo, 18.618-970, Brazil, rodriguesdn@yahoo.com.br Prof. Ângela M Soares, Universidade Estadual Paulista Júlio de Mesquita Filho, Departamento de Microbiologia e Imunologia, Botucatu, São Paulo, 18.618-970, Brazil, acsoares@ibb.unesp.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 Daniela R Rodrigues Reginaldo K Fernandes Helanderson A Balderramas Tatiana F Bachiega Sueli A Calvi Luciane A Dias-Melicio Marcimara Penitenti Maura R Ikoma Ângela M Soares Google Daniela R Rodrigues Reginaldo K Fernandes Helanderson A Balderramas Tatiana F Bachiega Sueli A Calvi Luciane A Dias-Melicio Marcimara Penitenti Maura R Ikoma Ângela M Soares Google Scholar Daniela R Rodrigues Reginaldo K Fernandes Helanderson A Balderramas Tatiana F Bachiega Sueli A Calvi Luciane A Dias-Melicio Marcimara Penitenti Maura R Ikoma Ângela M Soares PubMed Daniela R Rodrigues Reginaldo K Fernandes Helanderson A Balderramas Tatiana F Bachiega Sueli A Calvi Luciane A Dias-Melicio Marcimara Penitenti Maura R Ikoma Ângela M Soares 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.

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