Role of TLR2 and TLR4 in Human Neutrophil Functions Against Paracoccidioides brasiliensis

Detalhes bibliográficos
Autor(a) principal: Acorci-Valerio, M. J. [UNESP]
Data de Publicação: 2010
Outros Autores: 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]
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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spelling 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
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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)
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instname_str Universidade Estadual Paulista (UNESP)
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