Upregulation of reactive oxygen species generation and phagocytosis, and increased apoptosis in human neutrophils during severe sepsis and septic shock
Autor(a) principal: | |
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Data de Publicação: | 2003 |
Outros Autores: | , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://repositorio.unifesp.br/handle/11600/27377 http://dx.doi.org/10.1097/01.shk.0000079425.52617.db |
Resumo: | We evaluated neutrophil activation by measuring its phagocytic ability and oxidative burst activity in 16 patients with sepsis and 16 healthy volunteers. We also focused on neutrophil apoptosis as a regulatory mechanism of the inflammatory response. Neutrophil phagocytosis was evaluated by the detection of propidium iodide (PI)-labeled Staphylococcus aureus added to whole blood. Reactive oxygen species (ROS) formation was quantified by measuring the oxidation of 2',7' dichlorofluorescein diacetate (DCFH-DA) at baseline and after cell stimulation with phorbol myristate acetate (PMA), and bacterial cells (killed S. aureus) or products (lipopolysaccharide [LPS] and N-formyl-methionyl-leucylphenylalanine [FMLP]). Apoptosis was assessed in neutrophils stained with annexin V and Pl. Neutrophil phagocytic ability was increased in patients with sepsis compared with healthy controls (median geometric mean fluorescence intensity [GMFI] was 101.9 and 54.7, respectively; P = 0.05). ROS formation was enhanced in patients with sepsis compared with healthy volunteers at baseline (median GMFI 275.6 and 52.1, respectively; P < 0.001), and after stimulation with S. aureus (median GMFI 2395.8 and 454.9, respectively; P < 0.001), PMA (median GMFI 1120.6 and 307.5, respectively; P = 0.003), FMLP (median GMFl 792.4 and 123.2, respectively; P < 0.001), and LPS (median GMFI 624.8 and 144.8, respectively; P < 0.001). Early neutrophil apoptosis was increased in patients with sepsis compared with healthy volunteers (median 11.3% and 9.1%, respectively; P = 0.03). These data demonstrate that neutrophil function is enhanced in patients with sepsis. Additionally, circulating neutrophils from patients with sepsis presented with increased early apoptosis, which may be consequence of a regulatory mechanism of the inflammatory response. |
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Martins, Paulo Sergio [UNIFESP]Kallas, Esper Georges [UNIFESP]Cendoroglo Neto, Miguel [UNIFESP]Dalboni, Maria Aparecida [UNIFESP]Blecher, S.Salomão, Reinaldo [UNIFESP]Universidade Federal de São Paulo (UNIFESP)Santa Marcelina Hosp2016-01-24T12:34:00Z2016-01-24T12:34:00Z2003-09-01Shock. Philadelphia: Lippincott Williams & Wilkins, v. 20, n. 3, p. 208-212, 2003.1073-2322http://repositorio.unifesp.br/handle/11600/27377http://dx.doi.org/10.1097/01.shk.0000079425.52617.db10.1097/01.shk.0000079425.52617.dbWOS:000184841100002We evaluated neutrophil activation by measuring its phagocytic ability and oxidative burst activity in 16 patients with sepsis and 16 healthy volunteers. We also focused on neutrophil apoptosis as a regulatory mechanism of the inflammatory response. Neutrophil phagocytosis was evaluated by the detection of propidium iodide (PI)-labeled Staphylococcus aureus added to whole blood. Reactive oxygen species (ROS) formation was quantified by measuring the oxidation of 2',7' dichlorofluorescein diacetate (DCFH-DA) at baseline and after cell stimulation with phorbol myristate acetate (PMA), and bacterial cells (killed S. aureus) or products (lipopolysaccharide [LPS] and N-formyl-methionyl-leucylphenylalanine [FMLP]). Apoptosis was assessed in neutrophils stained with annexin V and Pl. Neutrophil phagocytic ability was increased in patients with sepsis compared with healthy controls (median geometric mean fluorescence intensity [GMFI] was 101.9 and 54.7, respectively; P = 0.05). ROS formation was enhanced in patients with sepsis compared with healthy volunteers at baseline (median GMFI 275.6 and 52.1, respectively; P < 0.001), and after stimulation with S. aureus (median GMFI 2395.8 and 454.9, respectively; P < 0.001), PMA (median GMFI 1120.6 and 307.5, respectively; P = 0.003), FMLP (median GMFl 792.4 and 123.2, respectively; P < 0.001), and LPS (median GMFI 624.8 and 144.8, respectively; P < 0.001). Early neutrophil apoptosis was increased in patients with sepsis compared with healthy volunteers (median 11.3% and 9.1%, respectively; P = 0.03). These data demonstrate that neutrophil function is enhanced in patients with sepsis. Additionally, circulating neutrophils from patients with sepsis presented with increased early apoptosis, which may be consequence of a regulatory mechanism of the inflammatory response.Universidade Federal de São Paulo, Immunol Lab, Div Infect Dis, Escola Paulista Med, BR-04039032 São Paulo, BrazilUniversidade Federal de São Paulo, Div Nephrol, Escola Paulista Med, BR-04039 São Paulo, BrazilSanta Marcelina Hosp, Intens Care Unit, São Paulo, BrazilUniversidade Federal de São Paulo, Immunol Lab, Div Infect Dis, Escola Paulista Med, BR-04039032 São Paulo, BrazilUniversidade Federal de São Paulo, Div Nephrol, Escola Paulista Med, BR-04039 São Paulo, BrazilWeb of Science208-212engLippincott Williams & WilkinsShockoxidative metabolismflow cytometryinflammatory responseS. aureusLPSUpregulation of reactive oxygen species generation and phagocytosis, and increased apoptosis in human neutrophils during severe sepsis and septic shockinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP11600/273772022-06-02 09:27:09.583metadata only accessoai:repositorio.unifesp.br:11600/27377Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652023-05-25T12:15:21.262951Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.en.fl_str_mv |
Upregulation of reactive oxygen species generation and phagocytosis, and increased apoptosis in human neutrophils during severe sepsis and septic shock |
title |
Upregulation of reactive oxygen species generation and phagocytosis, and increased apoptosis in human neutrophils during severe sepsis and septic shock |
spellingShingle |
Upregulation of reactive oxygen species generation and phagocytosis, and increased apoptosis in human neutrophils during severe sepsis and septic shock Martins, Paulo Sergio [UNIFESP] oxidative metabolism flow cytometry inflammatory response S. aureus LPS |
title_short |
Upregulation of reactive oxygen species generation and phagocytosis, and increased apoptosis in human neutrophils during severe sepsis and septic shock |
title_full |
Upregulation of reactive oxygen species generation and phagocytosis, and increased apoptosis in human neutrophils during severe sepsis and septic shock |
title_fullStr |
Upregulation of reactive oxygen species generation and phagocytosis, and increased apoptosis in human neutrophils during severe sepsis and septic shock |
title_full_unstemmed |
Upregulation of reactive oxygen species generation and phagocytosis, and increased apoptosis in human neutrophils during severe sepsis and septic shock |
title_sort |
Upregulation of reactive oxygen species generation and phagocytosis, and increased apoptosis in human neutrophils during severe sepsis and septic shock |
author |
Martins, Paulo Sergio [UNIFESP] |
author_facet |
Martins, Paulo Sergio [UNIFESP] Kallas, Esper Georges [UNIFESP] Cendoroglo Neto, Miguel [UNIFESP] Dalboni, Maria Aparecida [UNIFESP] Blecher, S. Salomão, Reinaldo [UNIFESP] |
author_role |
author |
author2 |
Kallas, Esper Georges [UNIFESP] Cendoroglo Neto, Miguel [UNIFESP] Dalboni, Maria Aparecida [UNIFESP] Blecher, S. Salomão, Reinaldo [UNIFESP] |
author2_role |
author author author author author |
dc.contributor.institution.none.fl_str_mv |
Universidade Federal de São Paulo (UNIFESP) Santa Marcelina Hosp |
dc.contributor.author.fl_str_mv |
Martins, Paulo Sergio [UNIFESP] Kallas, Esper Georges [UNIFESP] Cendoroglo Neto, Miguel [UNIFESP] Dalboni, Maria Aparecida [UNIFESP] Blecher, S. Salomão, Reinaldo [UNIFESP] |
dc.subject.eng.fl_str_mv |
oxidative metabolism flow cytometry inflammatory response S. aureus LPS |
topic |
oxidative metabolism flow cytometry inflammatory response S. aureus LPS |
description |
We evaluated neutrophil activation by measuring its phagocytic ability and oxidative burst activity in 16 patients with sepsis and 16 healthy volunteers. We also focused on neutrophil apoptosis as a regulatory mechanism of the inflammatory response. Neutrophil phagocytosis was evaluated by the detection of propidium iodide (PI)-labeled Staphylococcus aureus added to whole blood. Reactive oxygen species (ROS) formation was quantified by measuring the oxidation of 2',7' dichlorofluorescein diacetate (DCFH-DA) at baseline and after cell stimulation with phorbol myristate acetate (PMA), and bacterial cells (killed S. aureus) or products (lipopolysaccharide [LPS] and N-formyl-methionyl-leucylphenylalanine [FMLP]). Apoptosis was assessed in neutrophils stained with annexin V and Pl. Neutrophil phagocytic ability was increased in patients with sepsis compared with healthy controls (median geometric mean fluorescence intensity [GMFI] was 101.9 and 54.7, respectively; P = 0.05). ROS formation was enhanced in patients with sepsis compared with healthy volunteers at baseline (median GMFI 275.6 and 52.1, respectively; P < 0.001), and after stimulation with S. aureus (median GMFI 2395.8 and 454.9, respectively; P < 0.001), PMA (median GMFI 1120.6 and 307.5, respectively; P = 0.003), FMLP (median GMFl 792.4 and 123.2, respectively; P < 0.001), and LPS (median GMFI 624.8 and 144.8, respectively; P < 0.001). Early neutrophil apoptosis was increased in patients with sepsis compared with healthy volunteers (median 11.3% and 9.1%, respectively; P = 0.03). These data demonstrate that neutrophil function is enhanced in patients with sepsis. Additionally, circulating neutrophils from patients with sepsis presented with increased early apoptosis, which may be consequence of a regulatory mechanism of the inflammatory response. |
publishDate |
2003 |
dc.date.issued.fl_str_mv |
2003-09-01 |
dc.date.accessioned.fl_str_mv |
2016-01-24T12:34:00Z |
dc.date.available.fl_str_mv |
2016-01-24T12:34:00Z |
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.citation.fl_str_mv |
Shock. Philadelphia: Lippincott Williams & Wilkins, v. 20, n. 3, p. 208-212, 2003. |
dc.identifier.uri.fl_str_mv |
http://repositorio.unifesp.br/handle/11600/27377 http://dx.doi.org/10.1097/01.shk.0000079425.52617.db |
dc.identifier.issn.none.fl_str_mv |
1073-2322 |
dc.identifier.doi.none.fl_str_mv |
10.1097/01.shk.0000079425.52617.db |
dc.identifier.wos.none.fl_str_mv |
WOS:000184841100002 |
identifier_str_mv |
Shock. Philadelphia: Lippincott Williams & Wilkins, v. 20, n. 3, p. 208-212, 2003. 1073-2322 10.1097/01.shk.0000079425.52617.db WOS:000184841100002 |
url |
http://repositorio.unifesp.br/handle/11600/27377 http://dx.doi.org/10.1097/01.shk.0000079425.52617.db |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.ispartof.none.fl_str_mv |
Shock |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
208-212 |
dc.publisher.none.fl_str_mv |
Lippincott Williams & Wilkins |
publisher.none.fl_str_mv |
Lippincott Williams & Wilkins |
dc.source.none.fl_str_mv |
reponame:Repositório Institucional da UNIFESP instname:Universidade Federal de São Paulo (UNIFESP) instacron:UNIFESP |
instname_str |
Universidade Federal de São Paulo (UNIFESP) |
instacron_str |
UNIFESP |
institution |
UNIFESP |
reponame_str |
Repositório Institucional da UNIFESP |
collection |
Repositório Institucional da UNIFESP |
repository.name.fl_str_mv |
Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP) |
repository.mail.fl_str_mv |
|
_version_ |
1783460268220612608 |