Role of TLR2 and TLR4 in Human Neutrophil Functions Against Paracoccidioides brasiliensis
Autor(a) principal: | |
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Data de Publicação: | 2010 |
Outros Autores: | , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNESP |
Texto Completo: | http://dx.doi.org/10.1111/j.1365-3083.2009.02351.x http://hdl.handle.net/11449/18284 |
Resumo: | In paracoccidioidomycosis, a systemic mycosis caused by the fungus Paracoccidioides brasiliensis (Pb), studies have focused on the role of neutrophils that are involved in primary response to the fungus. Neutrophil functions are regulated by pro- and anti-inflammatory cytokines. The molecular mechanisms involved in this process are not fully understood, but there are strong evidences about the involvement of toll-like receptors (TLR). We aimed at evaluating TLR2 and TLR4 expression on human neutrophils activated with GM-CSF, IL-15, TNF-alpha or IFN-gamma and challenged with a virulent strain of P. brasiliensis (Pb18). Moreover, we asked if these receptors have a role on fungicidal activity, H(2)O(2) and IL-6, IL-8, TNF-alpha and IL-10 production by activated and challenged cells. All cytokines increased TLR2 and TLR4 expression. Pb18 also increased TLR2 expression inducing an additional effect to that of cytokines. on the contrary, it inhibited TLR4 expression. All cytokines increased neutrophil fungicidal activity and H(2)O(2) production, but this process was not associated with TLR2 or TLR4. Neutrophils activation with GM-CSF and TNF-alpha resulted in a significative increase in IL-8 production, while IL-15 and IFN-gamma have no effect. Pb18 alone also increased IL-8 production. None of the cytokines activated neutrophils for IL-10 release. This cytokine was only detected after Pb18 challenge. Interestingly, IL-8 and IL-10 production involved TLR2 and mainly TLR4 modulation. Our data suggest that Pb18 uses TLR4 to gain access to human neutrophils. This interaction results in IL-8 and IL-10 production that may be considered as a pathogenic mechanism in paracoccidioidomycosis. |
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Role of TLR2 and TLR4 in Human Neutrophil Functions Against Paracoccidioides brasiliensisIn paracoccidioidomycosis, a systemic mycosis caused by the fungus Paracoccidioides brasiliensis (Pb), studies have focused on the role of neutrophils that are involved in primary response to the fungus. Neutrophil functions are regulated by pro- and anti-inflammatory cytokines. The molecular mechanisms involved in this process are not fully understood, but there are strong evidences about the involvement of toll-like receptors (TLR). We aimed at evaluating TLR2 and TLR4 expression on human neutrophils activated with GM-CSF, IL-15, TNF-alpha or IFN-gamma and challenged with a virulent strain of P. brasiliensis (Pb18). Moreover, we asked if these receptors have a role on fungicidal activity, H(2)O(2) and IL-6, IL-8, TNF-alpha and IL-10 production by activated and challenged cells. All cytokines increased TLR2 and TLR4 expression. Pb18 also increased TLR2 expression inducing an additional effect to that of cytokines. on the contrary, it inhibited TLR4 expression. All cytokines increased neutrophil fungicidal activity and H(2)O(2) production, but this process was not associated with TLR2 or TLR4. Neutrophils activation with GM-CSF and TNF-alpha resulted in a significative increase in IL-8 production, while IL-15 and IFN-gamma have no effect. Pb18 alone also increased IL-8 production. None of the cytokines activated neutrophils for IL-10 release. This cytokine was only detected after Pb18 challenge. Interestingly, IL-8 and IL-10 production involved TLR2 and mainly TLR4 modulation. Our data suggest that Pb18 uses TLR4 to gain access to human neutrophils. This interaction results in IL-8 and IL-10 production that may be considered as a pathogenic mechanism in paracoccidioidomycosis.Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)São Paulo State Univ, Dept Microbiol & Immunol, Biosci Inst, BR-18618000 Botucatu, SP, BrazilSão Paulo State Univ, Sch Med, Botucatu Blood Ctr, BR-18618000 Botucatu, SP, BrazilSão Paulo State Univ, Dept Microbiol & Immunol, Biosci Inst, BR-18618000 Botucatu, SP, BrazilSão Paulo State Univ, Sch Med, Botucatu Blood Ctr, BR-18618000 Botucatu, SP, BrazilCNPq: 307009/207-6Wiley-Blackwell Publishing, IncUniversidade Estadual Paulista (Unesp)Acorci-Valerio, M. J. [UNESP]Bordon-Graciani, A. P. [UNESP]Dias-Melicio, L. A. [UNESP]Golim, M. de Assis [UNESP]Nakaira-Takahagi, E. [UNESP]de Campos Soares, A. M. V. [UNESP]2014-05-20T13:51:13Z2014-05-20T13:51:13Z2010-02-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article99-108application/pdfhttp://dx.doi.org/10.1111/j.1365-3083.2009.02351.xScandinavian Journal of Immunology. Malden: Wiley-blackwell Publishing, Inc, v. 71, n. 2, p. 99-108, 2010.0300-9475http://hdl.handle.net/11449/1828410.1111/j.1365-3083.2009.02351.xWOS:000273688300005WOS000273688300005.pdfWeb of Sciencereponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengScandinavian Journal of Immunology2.3140,891info:eu-repo/semantics/openAccess2024-01-03T06:27:24Zoai:repositorio.unesp.br:11449/18284Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-05T22:04:06.858176Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false |
dc.title.none.fl_str_mv |
Role of TLR2 and TLR4 in Human Neutrophil Functions Against Paracoccidioides brasiliensis |
title |
Role of TLR2 and TLR4 in Human Neutrophil Functions Against Paracoccidioides brasiliensis |
spellingShingle |
Role of TLR2 and TLR4 in Human Neutrophil Functions Against Paracoccidioides brasiliensis Acorci-Valerio, M. J. [UNESP] |
title_short |
Role of TLR2 and TLR4 in Human Neutrophil Functions Against Paracoccidioides brasiliensis |
title_full |
Role of TLR2 and TLR4 in Human Neutrophil Functions Against Paracoccidioides brasiliensis |
title_fullStr |
Role of TLR2 and TLR4 in Human Neutrophil Functions Against Paracoccidioides brasiliensis |
title_full_unstemmed |
Role of TLR2 and TLR4 in Human Neutrophil Functions Against Paracoccidioides brasiliensis |
title_sort |
Role of TLR2 and TLR4 in Human Neutrophil Functions Against Paracoccidioides brasiliensis |
author |
Acorci-Valerio, M. J. [UNESP] |
author_facet |
Acorci-Valerio, M. J. [UNESP] Bordon-Graciani, A. P. [UNESP] Dias-Melicio, L. A. [UNESP] Golim, M. de Assis [UNESP] Nakaira-Takahagi, E. [UNESP] de Campos Soares, A. M. V. [UNESP] |
author_role |
author |
author2 |
Bordon-Graciani, A. P. [UNESP] Dias-Melicio, L. A. [UNESP] Golim, M. de Assis [UNESP] Nakaira-Takahagi, E. [UNESP] de Campos Soares, A. M. V. [UNESP] |
author2_role |
author author author author author |
dc.contributor.none.fl_str_mv |
Universidade Estadual Paulista (Unesp) |
dc.contributor.author.fl_str_mv |
Acorci-Valerio, M. J. [UNESP] Bordon-Graciani, A. P. [UNESP] Dias-Melicio, L. A. [UNESP] Golim, M. de Assis [UNESP] Nakaira-Takahagi, E. [UNESP] de Campos Soares, A. M. V. [UNESP] |
description |
In paracoccidioidomycosis, a systemic mycosis caused by the fungus Paracoccidioides brasiliensis (Pb), studies have focused on the role of neutrophils that are involved in primary response to the fungus. Neutrophil functions are regulated by pro- and anti-inflammatory cytokines. The molecular mechanisms involved in this process are not fully understood, but there are strong evidences about the involvement of toll-like receptors (TLR). We aimed at evaluating TLR2 and TLR4 expression on human neutrophils activated with GM-CSF, IL-15, TNF-alpha or IFN-gamma and challenged with a virulent strain of P. brasiliensis (Pb18). Moreover, we asked if these receptors have a role on fungicidal activity, H(2)O(2) and IL-6, IL-8, TNF-alpha and IL-10 production by activated and challenged cells. All cytokines increased TLR2 and TLR4 expression. Pb18 also increased TLR2 expression inducing an additional effect to that of cytokines. on the contrary, it inhibited TLR4 expression. All cytokines increased neutrophil fungicidal activity and H(2)O(2) production, but this process was not associated with TLR2 or TLR4. Neutrophils activation with GM-CSF and TNF-alpha resulted in a significative increase in IL-8 production, while IL-15 and IFN-gamma have no effect. Pb18 alone also increased IL-8 production. None of the cytokines activated neutrophils for IL-10 release. This cytokine was only detected after Pb18 challenge. Interestingly, IL-8 and IL-10 production involved TLR2 and mainly TLR4 modulation. Our data suggest that Pb18 uses TLR4 to gain access to human neutrophils. This interaction results in IL-8 and IL-10 production that may be considered as a pathogenic mechanism in paracoccidioidomycosis. |
publishDate |
2010 |
dc.date.none.fl_str_mv |
2010-02-01 2014-05-20T13:51:13Z 2014-05-20T13:51:13Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://dx.doi.org/10.1111/j.1365-3083.2009.02351.x Scandinavian Journal of Immunology. Malden: Wiley-blackwell Publishing, Inc, v. 71, n. 2, p. 99-108, 2010. 0300-9475 http://hdl.handle.net/11449/18284 10.1111/j.1365-3083.2009.02351.x WOS:000273688300005 WOS000273688300005.pdf |
url |
http://dx.doi.org/10.1111/j.1365-3083.2009.02351.x http://hdl.handle.net/11449/18284 |
identifier_str_mv |
Scandinavian Journal of Immunology. Malden: Wiley-blackwell Publishing, Inc, v. 71, n. 2, p. 99-108, 2010. 0300-9475 10.1111/j.1365-3083.2009.02351.x WOS:000273688300005 WOS000273688300005.pdf |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Scandinavian Journal of Immunology 2.314 0,891 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
99-108 application/pdf |
dc.publisher.none.fl_str_mv |
Wiley-Blackwell Publishing, Inc |
publisher.none.fl_str_mv |
Wiley-Blackwell Publishing, Inc |
dc.source.none.fl_str_mv |
Web of Science reponame:Repositório Institucional da UNESP instname:Universidade Estadual Paulista (UNESP) instacron:UNESP |
instname_str |
Universidade Estadual Paulista (UNESP) |
instacron_str |
UNESP |
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UNESP |
reponame_str |
Repositório Institucional da UNESP |
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Repositório Institucional da UNESP |
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Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP) |
repository.mail.fl_str_mv |
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1808129388651216896 |