Bordetella parapertussis Circumvents Neutrophil Extracellular Bactericidal Mechanisms
- Autores
- Gorgojo, Juan Pablo; Scharrig, Emilia; Gómez, Ricardo Martín; Harvill, Eric T.; Rodríguez, María Eugenia
- Año de publicación
- 2017
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- B. parapertussis is a whooping cough etiological agent with the ability to evade the immune response induced by pertussis vaccines. We previously demonstrated that in the absence of opsonic antibodies B. parapertussis hampers phagocytosis by neutrophils and macrophages and, when phagocytosed, blocks intracellular killing by interfering with phagolysosomal fusion. But neutrophils can kill and/or immobilize extracellular bacteria through nonphagocytic mechanisms such as degranulation and neutrophil extracellular traps (NETs). In this study we demonstrated that B. parapertussis also has the ability to circumvent these two neutrophil extracellular bactericidal activities. The lack of neutrophil degranulation was found dependent on the O antigen that targets the bacteria to cell lipid rafts, eventually avoiding the fusion of nascent phagosomes with specific and azurophilic granules. IgG opsonization overcame this inhibition of neutrophil degranulation. We further observed that B. parapertussis did not induce NETs release in resting neutrophils and inhibited NETs formation in response to phorbol myristate acetate (PMA) stimulation by a mechanism dependent on adenylate cyclase toxin (CyaA)-mediated inhibition of reactive oxygen species (ROS) generation. Thus, B. parapertussis modulates neutrophil bactericidal activity through two different mechanisms, one related to the lack of proper NETs-inducer stimuli and the other one related to an active inhibitory mechanism. Together with previous results these data suggest that B. parapertussis has the ability to subvert the main neutrophil bactericidal functions, inhibiting efficient clearance in non-immune hosts.
Centro de Investigación y Desarrollo en Fermentaciones Industriales
Instituto de Biotecnologia y Biologia Molecular - Materia
-
Biología
Bordetella pertussis
Neutrophils - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- http://creativecommons.org/licenses/by/4.0/
- Repositorio
- Institución
- Universidad Nacional de La Plata
- OAI Identificador
- oai:sedici.unlp.edu.ar:10915/87579
Ver los metadatos del registro completo
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Bordetella parapertussis Circumvents Neutrophil Extracellular Bactericidal MechanismsGorgojo, Juan PabloScharrig, EmiliaGómez, Ricardo MartínHarvill, Eric T.Rodríguez, María EugeniaBiologíaBordetella pertussisNeutrophilsB. parapertussis is a whooping cough etiological agent with the ability to evade the immune response induced by pertussis vaccines. We previously demonstrated that in the absence of opsonic antibodies B. parapertussis hampers phagocytosis by neutrophils and macrophages and, when phagocytosed, blocks intracellular killing by interfering with phagolysosomal fusion. But neutrophils can kill and/or immobilize extracellular bacteria through nonphagocytic mechanisms such as degranulation and neutrophil extracellular traps (NETs). In this study we demonstrated that B. parapertussis also has the ability to circumvent these two neutrophil extracellular bactericidal activities. The lack of neutrophil degranulation was found dependent on the O antigen that targets the bacteria to cell lipid rafts, eventually avoiding the fusion of nascent phagosomes with specific and azurophilic granules. IgG opsonization overcame this inhibition of neutrophil degranulation. We further observed that B. parapertussis did not induce NETs release in resting neutrophils and inhibited NETs formation in response to phorbol myristate acetate (PMA) stimulation by a mechanism dependent on adenylate cyclase toxin (CyaA)-mediated inhibition of reactive oxygen species (ROS) generation. Thus, B. parapertussis modulates neutrophil bactericidal activity through two different mechanisms, one related to the lack of proper NETs-inducer stimuli and the other one related to an active inhibitory mechanism. Together with previous results these data suggest that B. parapertussis has the ability to subvert the main neutrophil bactericidal functions, inhibiting efficient clearance in non-immune hosts.Centro de Investigación y Desarrollo en Fermentaciones IndustrialesInstituto de Biotecnologia y Biologia Molecular2017info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionArticulohttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttp://sedici.unlp.edu.ar/handle/10915/87579enginfo:eu-repo/semantics/altIdentifier/issn/1932-6203info:eu-repo/semantics/altIdentifier/doi/10.1371/journal.pone.0169936info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by/4.0/Creative Commons Attribution 4.0 International (CC BY 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-09-29T11:17:15Zoai:sedici.unlp.edu.ar:10915/87579Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-29 11:17:15.359SEDICI (UNLP) - Universidad Nacional de La Platafalse |
dc.title.none.fl_str_mv |
Bordetella parapertussis Circumvents Neutrophil Extracellular Bactericidal Mechanisms |
title |
Bordetella parapertussis Circumvents Neutrophil Extracellular Bactericidal Mechanisms |
spellingShingle |
Bordetella parapertussis Circumvents Neutrophil Extracellular Bactericidal Mechanisms Gorgojo, Juan Pablo Biología Bordetella pertussis Neutrophils |
title_short |
Bordetella parapertussis Circumvents Neutrophil Extracellular Bactericidal Mechanisms |
title_full |
Bordetella parapertussis Circumvents Neutrophil Extracellular Bactericidal Mechanisms |
title_fullStr |
Bordetella parapertussis Circumvents Neutrophil Extracellular Bactericidal Mechanisms |
title_full_unstemmed |
Bordetella parapertussis Circumvents Neutrophil Extracellular Bactericidal Mechanisms |
title_sort |
Bordetella parapertussis Circumvents Neutrophil Extracellular Bactericidal Mechanisms |
dc.creator.none.fl_str_mv |
Gorgojo, Juan Pablo Scharrig, Emilia Gómez, Ricardo Martín Harvill, Eric T. Rodríguez, María Eugenia |
author |
Gorgojo, Juan Pablo |
author_facet |
Gorgojo, Juan Pablo Scharrig, Emilia Gómez, Ricardo Martín Harvill, Eric T. Rodríguez, María Eugenia |
author_role |
author |
author2 |
Scharrig, Emilia Gómez, Ricardo Martín Harvill, Eric T. Rodríguez, María Eugenia |
author2_role |
author author author author |
dc.subject.none.fl_str_mv |
Biología Bordetella pertussis Neutrophils |
topic |
Biología Bordetella pertussis Neutrophils |
dc.description.none.fl_txt_mv |
B. parapertussis is a whooping cough etiological agent with the ability to evade the immune response induced by pertussis vaccines. We previously demonstrated that in the absence of opsonic antibodies B. parapertussis hampers phagocytosis by neutrophils and macrophages and, when phagocytosed, blocks intracellular killing by interfering with phagolysosomal fusion. But neutrophils can kill and/or immobilize extracellular bacteria through nonphagocytic mechanisms such as degranulation and neutrophil extracellular traps (NETs). In this study we demonstrated that B. parapertussis also has the ability to circumvent these two neutrophil extracellular bactericidal activities. The lack of neutrophil degranulation was found dependent on the O antigen that targets the bacteria to cell lipid rafts, eventually avoiding the fusion of nascent phagosomes with specific and azurophilic granules. IgG opsonization overcame this inhibition of neutrophil degranulation. We further observed that B. parapertussis did not induce NETs release in resting neutrophils and inhibited NETs formation in response to phorbol myristate acetate (PMA) stimulation by a mechanism dependent on adenylate cyclase toxin (CyaA)-mediated inhibition of reactive oxygen species (ROS) generation. Thus, B. parapertussis modulates neutrophil bactericidal activity through two different mechanisms, one related to the lack of proper NETs-inducer stimuli and the other one related to an active inhibitory mechanism. Together with previous results these data suggest that B. parapertussis has the ability to subvert the main neutrophil bactericidal functions, inhibiting efficient clearance in non-immune hosts. Centro de Investigación y Desarrollo en Fermentaciones Industriales Instituto de Biotecnologia y Biologia Molecular |
description |
B. parapertussis is a whooping cough etiological agent with the ability to evade the immune response induced by pertussis vaccines. We previously demonstrated that in the absence of opsonic antibodies B. parapertussis hampers phagocytosis by neutrophils and macrophages and, when phagocytosed, blocks intracellular killing by interfering with phagolysosomal fusion. But neutrophils can kill and/or immobilize extracellular bacteria through nonphagocytic mechanisms such as degranulation and neutrophil extracellular traps (NETs). In this study we demonstrated that B. parapertussis also has the ability to circumvent these two neutrophil extracellular bactericidal activities. The lack of neutrophil degranulation was found dependent on the O antigen that targets the bacteria to cell lipid rafts, eventually avoiding the fusion of nascent phagosomes with specific and azurophilic granules. IgG opsonization overcame this inhibition of neutrophil degranulation. We further observed that B. parapertussis did not induce NETs release in resting neutrophils and inhibited NETs formation in response to phorbol myristate acetate (PMA) stimulation by a mechanism dependent on adenylate cyclase toxin (CyaA)-mediated inhibition of reactive oxygen species (ROS) generation. Thus, B. parapertussis modulates neutrophil bactericidal activity through two different mechanisms, one related to the lack of proper NETs-inducer stimuli and the other one related to an active inhibitory mechanism. Together with previous results these data suggest that B. parapertussis has the ability to subvert the main neutrophil bactericidal functions, inhibiting efficient clearance in non-immune hosts. |
publishDate |
2017 |
dc.date.none.fl_str_mv |
2017 |
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eng |
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