Neutrophilic cell-free exudate induces antinociception mediate by the protein S100A9
Autor(a) principal: | |
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Data de Publicação: | 2006 |
Outros Autores: | , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://repositorio.unifesp.br/handle/11600/28612 http://dx.doi.org/10.1155/MI/2006/36765 |
Resumo: | Calcium-binding protein S100A9 (MRP-14) induces antinociceptive effect in an experimental model of painful sensibility and participates of antinociception observed during neutrophilic peritonitis induced by glycogen or carrageenan in mice. in this study, the direct antinociceptive role of the protein S100A9 in neutrophilic cell-free exudates obtained of mice injected with glycogen was investigated. Mice were intraperitoneally injected with a glycogen solution, and after 4, 8, 24, and 48 hours, either the pattern of cell migration of the peritoneal exudate or the nociceptive response of animals was evaluated. the glycogen-induced neutrophilic peritonitis evoked antinociception 4 and 8 hours after inoculation of the irritant. Peritoneal cell-free exudates, collected in different times after the irritant injection, were transferred to naive animals which were submitted to the nociceptive test. the transference of exudates also induced antinociceptive effect, and neutralization of S100A9 activity by anti-S100A9 monoclonal antibody totally reverted this response. This effect was not observed when experiments were made 24 or 48 hours after glycogen injection. These results clearly indicate that S100A9 is secreted during glycogen-induced neutrophilic peritonitis, and that this protein is responsible by antinociception observed in the initial phase of inflammatory reaction. Thus, these data reinforce the hypothesis that the calcium-binding protein S100A9 participates of the endogenous control of inflammatory pain. |
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Pagano, Rosana L.Mariano, Mario [UNIFESP]Giorgi, RenataButantan InstUniversidade Federal de São Paulo (UNIFESP)Paulista Univ2016-01-24T12:38:14Z2016-01-24T12:38:14Z2006-01-01Mediators of Inflammation. New York: Hindawi Publishing Corporation, 6 p., 2006.0962-9351http://repositorio.unifesp.br/handle/11600/28612http://dx.doi.org/10.1155/MI/2006/36765WOS000242587800001.pdf10.1155/MI/2006/36765WOS:000242587800001Calcium-binding protein S100A9 (MRP-14) induces antinociceptive effect in an experimental model of painful sensibility and participates of antinociception observed during neutrophilic peritonitis induced by glycogen or carrageenan in mice. in this study, the direct antinociceptive role of the protein S100A9 in neutrophilic cell-free exudates obtained of mice injected with glycogen was investigated. Mice were intraperitoneally injected with a glycogen solution, and after 4, 8, 24, and 48 hours, either the pattern of cell migration of the peritoneal exudate or the nociceptive response of animals was evaluated. the glycogen-induced neutrophilic peritonitis evoked antinociception 4 and 8 hours after inoculation of the irritant. Peritoneal cell-free exudates, collected in different times after the irritant injection, were transferred to naive animals which were submitted to the nociceptive test. the transference of exudates also induced antinociceptive effect, and neutralization of S100A9 activity by anti-S100A9 monoclonal antibody totally reverted this response. This effect was not observed when experiments were made 24 or 48 hours after glycogen injection. These results clearly indicate that S100A9 is secreted during glycogen-induced neutrophilic peritonitis, and that this protein is responsible by antinociception observed in the initial phase of inflammatory reaction. Thus, these data reinforce the hypothesis that the calcium-binding protein S100A9 participates of the endogenous control of inflammatory pain.Butantan Inst, Lab Pathophysiol, BR-05503900 São Paulo, BrazilUniversidade Federal de São Paulo, Discipline Immunol, BR-04023062 São Paulo, BrazilPaulista Univ, Discipline Immunol, BR-04026002 São Paulo, BrazilUniversidade Federal de São Paulo, Discipline Immunol, BR-04023062 São Paulo, BrazilWeb of Science6engHindawi Publishing CorporationMediators of InflammationNeutrophilic cell-free exudate induces antinociception mediate by the protein S100A9info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESPORIGINALWOS000242587800001.pdfapplication/pdf1302293${dspace.ui.url}/bitstream/11600/28612/1/WOS000242587800001.pdf384e1582f3a43c90edd156d7078976aaMD51open accessTEXTWOS000242587800001.pdf.txtWOS000242587800001.pdf.txtExtracted texttext/plain28892${dspace.ui.url}/bitstream/11600/28612/2/WOS000242587800001.pdf.txt53ae87cef7f4107027a623cc6d87a827MD52open access11600/286122022-06-02 09:20:44.374open accessoai:repositorio.unifesp.br:11600/28612Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652023-05-25T12:15:08.544968Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.en.fl_str_mv |
Neutrophilic cell-free exudate induces antinociception mediate by the protein S100A9 |
title |
Neutrophilic cell-free exudate induces antinociception mediate by the protein S100A9 |
spellingShingle |
Neutrophilic cell-free exudate induces antinociception mediate by the protein S100A9 Pagano, Rosana L. |
title_short |
Neutrophilic cell-free exudate induces antinociception mediate by the protein S100A9 |
title_full |
Neutrophilic cell-free exudate induces antinociception mediate by the protein S100A9 |
title_fullStr |
Neutrophilic cell-free exudate induces antinociception mediate by the protein S100A9 |
title_full_unstemmed |
Neutrophilic cell-free exudate induces antinociception mediate by the protein S100A9 |
title_sort |
Neutrophilic cell-free exudate induces antinociception mediate by the protein S100A9 |
author |
Pagano, Rosana L. |
author_facet |
Pagano, Rosana L. Mariano, Mario [UNIFESP] Giorgi, Renata |
author_role |
author |
author2 |
Mariano, Mario [UNIFESP] Giorgi, Renata |
author2_role |
author author |
dc.contributor.institution.none.fl_str_mv |
Butantan Inst Universidade Federal de São Paulo (UNIFESP) Paulista Univ |
dc.contributor.author.fl_str_mv |
Pagano, Rosana L. Mariano, Mario [UNIFESP] Giorgi, Renata |
description |
Calcium-binding protein S100A9 (MRP-14) induces antinociceptive effect in an experimental model of painful sensibility and participates of antinociception observed during neutrophilic peritonitis induced by glycogen or carrageenan in mice. in this study, the direct antinociceptive role of the protein S100A9 in neutrophilic cell-free exudates obtained of mice injected with glycogen was investigated. Mice were intraperitoneally injected with a glycogen solution, and after 4, 8, 24, and 48 hours, either the pattern of cell migration of the peritoneal exudate or the nociceptive response of animals was evaluated. the glycogen-induced neutrophilic peritonitis evoked antinociception 4 and 8 hours after inoculation of the irritant. Peritoneal cell-free exudates, collected in different times after the irritant injection, were transferred to naive animals which were submitted to the nociceptive test. the transference of exudates also induced antinociceptive effect, and neutralization of S100A9 activity by anti-S100A9 monoclonal antibody totally reverted this response. This effect was not observed when experiments were made 24 or 48 hours after glycogen injection. These results clearly indicate that S100A9 is secreted during glycogen-induced neutrophilic peritonitis, and that this protein is responsible by antinociception observed in the initial phase of inflammatory reaction. Thus, these data reinforce the hypothesis that the calcium-binding protein S100A9 participates of the endogenous control of inflammatory pain. |
publishDate |
2006 |
dc.date.issued.fl_str_mv |
2006-01-01 |
dc.date.accessioned.fl_str_mv |
2016-01-24T12:38:14Z |
dc.date.available.fl_str_mv |
2016-01-24T12:38:14Z |
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info:eu-repo/semantics/publishedVersion |
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info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.citation.fl_str_mv |
Mediators of Inflammation. New York: Hindawi Publishing Corporation, 6 p., 2006. |
dc.identifier.uri.fl_str_mv |
http://repositorio.unifesp.br/handle/11600/28612 http://dx.doi.org/10.1155/MI/2006/36765 |
dc.identifier.issn.none.fl_str_mv |
0962-9351 |
dc.identifier.file.none.fl_str_mv |
WOS000242587800001.pdf |
dc.identifier.doi.none.fl_str_mv |
10.1155/MI/2006/36765 |
dc.identifier.wos.none.fl_str_mv |
WOS:000242587800001 |
identifier_str_mv |
Mediators of Inflammation. New York: Hindawi Publishing Corporation, 6 p., 2006. 0962-9351 WOS000242587800001.pdf 10.1155/MI/2006/36765 WOS:000242587800001 |
url |
http://repositorio.unifesp.br/handle/11600/28612 http://dx.doi.org/10.1155/MI/2006/36765 |
dc.language.iso.fl_str_mv |
eng |
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eng |
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Mediators of Inflammation |
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6 |
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Hindawi Publishing Corporation |
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Hindawi Publishing Corporation |
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