Activation of Human Neutrophils by the Anti-Inflammatory Mediator Esenbeckia leiocarpa Leads to Atypical Apoptosis
Despite the fact that Esenbeckia leiocarpa, a Brazilian plant, possesses potential anti-inflammatory properties, its effect in neutrophils, key players in inflammation, has never been investigated. In this study, a crude hydroalcoholic extract (CHE) was used to evaluate the potential toxic or agonis...
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Wiley
2012-01-01
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Series: | Mediators of Inflammation |
Online Access: | http://dx.doi.org/10.1155/2012/198382 |
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author | Rafael de Liz Heros Horst Moacir Geraldo Pizzolatti Tânia Silvia Fröde Denis Girard |
author_facet | Rafael de Liz Heros Horst Moacir Geraldo Pizzolatti Tânia Silvia Fröde Denis Girard |
author_sort | Rafael de Liz |
collection | DOAJ |
description | Despite the fact that Esenbeckia leiocarpa, a Brazilian plant, possesses potential anti-inflammatory properties, its effect in neutrophils, key players in inflammation, has never been investigated. In this study, a crude hydroalcoholic extract (CHE) was used to evaluate the potential toxic or agonistic effect of E. leiocarpa in human neutrophils. At a noncytotoxic concentration of 500 μg/mL, CHE increased actin polymerization and cell signaling events, especially p38 MAPK. Its modulatory activity on neutrophil cell apoptosis was investigated by cytology and by flow cytometry and, although CHE increased the apoptotic rate (by cytology) and increased annexin-V binding, it did not, unexpectedly, increase CD16 shedding. CHE increased the degradation of the cytoskeletal proteins gelsolin and paxillin but, surprisingly, not of vimentin. The proapoptotic activity of CHE was reversed by a pan-caspase inhibitor but not by a p38 inhibitor. We conclude that CHE is a novel human neutrophil agonist that induces apoptosis by a caspase-dependent and p38-independent mechanism in an atypical fashion based on its lack of effect on CD16 shedding and vimentin degradation. Since the resolution of inflammation occurs by elimination of apoptotic neutrophils, the ability of CHE to induce neutrophil apoptosis correlates well with its anti-inflammatory properties, as previously reported. |
format | Article |
id | doaj-art-3d6033e0732240c6bb6458e305a74607 |
institution | Kabale University |
issn | 0962-9351 1466-1861 |
language | English |
publishDate | 2012-01-01 |
publisher | Wiley |
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series | Mediators of Inflammation |
spelling | doaj-art-3d6033e0732240c6bb6458e305a746072025-02-03T01:02:28ZengWileyMediators of Inflammation0962-93511466-18612012-01-01201210.1155/2012/198382198382Activation of Human Neutrophils by the Anti-Inflammatory Mediator Esenbeckia leiocarpa Leads to Atypical ApoptosisRafael de Liz0Heros Horst1Moacir Geraldo Pizzolatti2Tânia Silvia Fröde3Denis Girard4Laboratoire de Recherche en Inflammation et Physiologie des Granulocytes, INRS-Institut Armand-Frappier, Université du Québec, 531 Boulevord des Prairies, Laval, QC, H7V 1B7, CanadaDepartment of Chemistry, Center of Physical and Mathematical Sciences, Federal University of Santa Catarina, Campus Universitário, Trindade, 88040-970 Florianópolis, SC, BrazilDepartment of Chemistry, Center of Physical and Mathematical Sciences, Federal University of Santa Catarina, Campus Universitário, Trindade, 88040-970 Florianópolis, SC, BrazilDepartment of Clinical Analysis, Center of Health Sciences, Federal University of Santa Catarina, Campus Universitário, Trindade, 88040-970 Florianópolis, SC, BrazilLaboratoire de Recherche en Inflammation et Physiologie des Granulocytes, INRS-Institut Armand-Frappier, Université du Québec, 531 Boulevord des Prairies, Laval, QC, H7V 1B7, CanadaDespite the fact that Esenbeckia leiocarpa, a Brazilian plant, possesses potential anti-inflammatory properties, its effect in neutrophils, key players in inflammation, has never been investigated. In this study, a crude hydroalcoholic extract (CHE) was used to evaluate the potential toxic or agonistic effect of E. leiocarpa in human neutrophils. At a noncytotoxic concentration of 500 μg/mL, CHE increased actin polymerization and cell signaling events, especially p38 MAPK. Its modulatory activity on neutrophil cell apoptosis was investigated by cytology and by flow cytometry and, although CHE increased the apoptotic rate (by cytology) and increased annexin-V binding, it did not, unexpectedly, increase CD16 shedding. CHE increased the degradation of the cytoskeletal proteins gelsolin and paxillin but, surprisingly, not of vimentin. The proapoptotic activity of CHE was reversed by a pan-caspase inhibitor but not by a p38 inhibitor. We conclude that CHE is a novel human neutrophil agonist that induces apoptosis by a caspase-dependent and p38-independent mechanism in an atypical fashion based on its lack of effect on CD16 shedding and vimentin degradation. Since the resolution of inflammation occurs by elimination of apoptotic neutrophils, the ability of CHE to induce neutrophil apoptosis correlates well with its anti-inflammatory properties, as previously reported.http://dx.doi.org/10.1155/2012/198382 |
spellingShingle | Rafael de Liz Heros Horst Moacir Geraldo Pizzolatti Tânia Silvia Fröde Denis Girard Activation of Human Neutrophils by the Anti-Inflammatory Mediator Esenbeckia leiocarpa Leads to Atypical Apoptosis Mediators of Inflammation |
title | Activation of Human Neutrophils by the Anti-Inflammatory Mediator Esenbeckia leiocarpa Leads to Atypical Apoptosis |
title_full | Activation of Human Neutrophils by the Anti-Inflammatory Mediator Esenbeckia leiocarpa Leads to Atypical Apoptosis |
title_fullStr | Activation of Human Neutrophils by the Anti-Inflammatory Mediator Esenbeckia leiocarpa Leads to Atypical Apoptosis |
title_full_unstemmed | Activation of Human Neutrophils by the Anti-Inflammatory Mediator Esenbeckia leiocarpa Leads to Atypical Apoptosis |
title_short | Activation of Human Neutrophils by the Anti-Inflammatory Mediator Esenbeckia leiocarpa Leads to Atypical Apoptosis |
title_sort | activation of human neutrophils by the anti inflammatory mediator esenbeckia leiocarpa leads to atypical apoptosis |
url | http://dx.doi.org/10.1155/2012/198382 |
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