Toxoplasma gondii infection modulate systemic allergic immune response in BALB/c mice
- Autores
- Fenoy, Ignacio Martín; Sánchez, Vanesa Roxana; Soto, Ariadna Soledad; Picchio, Mariano Sergio; Martín, Valentina; Goldman, Alejandra
- Año de publicación
- 2015
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- The increased prevalence of allergies in developed countries has been attributed to a reduced exposure to some microbes. In agreement with epidemiological studies, we previously showed that Toxoplasma gondii infection prevents allergic airway inflammation. The mechanisms would be related to the strong Th1 response induced by the parasite and to regulatory cell induction. Herein we further characterized whether T. gondii allergy modulation extents to a systemic level or if it is limited to the lung. Parasite infection before allergic sensitization resulted in a diminished Th2 cytokine response and, when sensitized during acute infection, an increased in TGF-β production was detected. Allergen specific T cell proliferation was also reduced. Sensitization during both acute and chronic phases of infection resulted in a decreased anaphylaxis reaction. Our results extend earlier work and show that, in addition to lung airway inflammation, T. gondii infection can suppress allergic responses at systemic level. These results open the possibility that this protozoan infection could modulate other allergic disorders such as atopic dermatitis or oral allergies. Understanding the mechanisms by which different microorganisms regulate inflammation may potentially lead to the development of strategies aimed to control atopic diseases.
Fil: Fenoy, Ignacio Martín. Universidad Nacional de San Martín. Escuela de Ciencia y Tecnología. Centro de Estudios en Salud y Medio Ambiente; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Sánchez, Vanesa Roxana. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional de San Martín. Escuela de Ciencia y Tecnología. Centro de Estudios en Salud y Medio Ambiente; Argentina
Fil: Soto, Ariadna Soledad. Universidad Nacional de San Martín. Escuela de Ciencia y Tecnología. Centro de Estudios en Salud y Medio Ambiente; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Picchio, Mariano Sergio. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional de San Martín. Escuela de Ciencia y Tecnología. Centro de Estudios en Salud y Medio Ambiente; Argentina
Fil: Martín, Valentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional de San Martín. Escuela de Ciencia y Tecnología. Centro de Estudios en Salud y Medio Ambiente; Argentina
Fil: Goldman, Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional de San Martín. Escuela de Ciencia y Tecnología. Centro de Estudios en Salud y Medio Ambiente; Argentina - Materia
-
ALLERGY
ANAPHYLAXIS
IMMUNE-MODULATION
INFECTION
TOXOPLASMA GONDII - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
- Repositorio
.jpg)
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/98633
Ver los metadatos del registro completo
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Toxoplasma gondii infection modulate systemic allergic immune response in BALB/c miceFenoy, Ignacio MartínSánchez, Vanesa RoxanaSoto, Ariadna SoledadPicchio, Mariano SergioMartín, ValentinaGoldman, AlejandraALLERGYANAPHYLAXISIMMUNE-MODULATIONINFECTIONTOXOPLASMA GONDIIhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3The increased prevalence of allergies in developed countries has been attributed to a reduced exposure to some microbes. In agreement with epidemiological studies, we previously showed that Toxoplasma gondii infection prevents allergic airway inflammation. The mechanisms would be related to the strong Th1 response induced by the parasite and to regulatory cell induction. Herein we further characterized whether T. gondii allergy modulation extents to a systemic level or if it is limited to the lung. Parasite infection before allergic sensitization resulted in a diminished Th2 cytokine response and, when sensitized during acute infection, an increased in TGF-β production was detected. Allergen specific T cell proliferation was also reduced. Sensitization during both acute and chronic phases of infection resulted in a decreased anaphylaxis reaction. Our results extend earlier work and show that, in addition to lung airway inflammation, T. gondii infection can suppress allergic responses at systemic level. These results open the possibility that this protozoan infection could modulate other allergic disorders such as atopic dermatitis or oral allergies. Understanding the mechanisms by which different microorganisms regulate inflammation may potentially lead to the development of strategies aimed to control atopic diseases.Fil: Fenoy, Ignacio Martín. Universidad Nacional de San Martín. Escuela de Ciencia y Tecnología. Centro de Estudios en Salud y Medio Ambiente; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Sánchez, Vanesa Roxana. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional de San Martín. Escuela de Ciencia y Tecnología. Centro de Estudios en Salud y Medio Ambiente; ArgentinaFil: Soto, Ariadna Soledad. Universidad Nacional de San Martín. Escuela de Ciencia y Tecnología. Centro de Estudios en Salud y Medio Ambiente; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Picchio, Mariano Sergio. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional de San Martín. Escuela de Ciencia y Tecnología. Centro de Estudios en Salud y Medio Ambiente; ArgentinaFil: Martín, Valentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional de San Martín. Escuela de Ciencia y Tecnología. Centro de Estudios en Salud y Medio Ambiente; ArgentinaFil: Goldman, Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional de San Martín. Escuela de Ciencia y Tecnología. Centro de Estudios en Salud y Medio Ambiente; ArgentinaAcademic Press Inc Elsevier Science2015-07info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/98633Fenoy, Ignacio Martín; Sánchez, Vanesa Roxana; Soto, Ariadna Soledad; Picchio, Mariano Sergio; Martín, Valentina; et al.; Toxoplasma gondii infection modulate systemic allergic immune response in BALB/c mice; Academic Press Inc Elsevier Science; Experimental Parasitology; 154; 7-2015; 47-500014-4894CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0014489415000909info:eu-repo/semantics/altIdentifier/doi/10.1016/j.exppara.2015.04.001info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-nd/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-22T12:04:31Zoai:ri.conicet.gov.ar:11336/98633instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-10-22 12:04:31.36CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
| dc.title.none.fl_str_mv |
Toxoplasma gondii infection modulate systemic allergic immune response in BALB/c mice |
| title |
Toxoplasma gondii infection modulate systemic allergic immune response in BALB/c mice |
| spellingShingle |
Toxoplasma gondii infection modulate systemic allergic immune response in BALB/c mice Fenoy, Ignacio Martín ALLERGY ANAPHYLAXIS IMMUNE-MODULATION INFECTION TOXOPLASMA GONDII |
| title_short |
Toxoplasma gondii infection modulate systemic allergic immune response in BALB/c mice |
| title_full |
Toxoplasma gondii infection modulate systemic allergic immune response in BALB/c mice |
| title_fullStr |
Toxoplasma gondii infection modulate systemic allergic immune response in BALB/c mice |
| title_full_unstemmed |
Toxoplasma gondii infection modulate systemic allergic immune response in BALB/c mice |
| title_sort |
Toxoplasma gondii infection modulate systemic allergic immune response in BALB/c mice |
| dc.creator.none.fl_str_mv |
Fenoy, Ignacio Martín Sánchez, Vanesa Roxana Soto, Ariadna Soledad Picchio, Mariano Sergio Martín, Valentina Goldman, Alejandra |
| author |
Fenoy, Ignacio Martín |
| author_facet |
Fenoy, Ignacio Martín Sánchez, Vanesa Roxana Soto, Ariadna Soledad Picchio, Mariano Sergio Martín, Valentina Goldman, Alejandra |
| author_role |
author |
| author2 |
Sánchez, Vanesa Roxana Soto, Ariadna Soledad Picchio, Mariano Sergio Martín, Valentina Goldman, Alejandra |
| author2_role |
author author author author author |
| dc.subject.none.fl_str_mv |
ALLERGY ANAPHYLAXIS IMMUNE-MODULATION INFECTION TOXOPLASMA GONDII |
| topic |
ALLERGY ANAPHYLAXIS IMMUNE-MODULATION INFECTION TOXOPLASMA GONDII |
| purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3 |
| dc.description.none.fl_txt_mv |
The increased prevalence of allergies in developed countries has been attributed to a reduced exposure to some microbes. In agreement with epidemiological studies, we previously showed that Toxoplasma gondii infection prevents allergic airway inflammation. The mechanisms would be related to the strong Th1 response induced by the parasite and to regulatory cell induction. Herein we further characterized whether T. gondii allergy modulation extents to a systemic level or if it is limited to the lung. Parasite infection before allergic sensitization resulted in a diminished Th2 cytokine response and, when sensitized during acute infection, an increased in TGF-β production was detected. Allergen specific T cell proliferation was also reduced. Sensitization during both acute and chronic phases of infection resulted in a decreased anaphylaxis reaction. Our results extend earlier work and show that, in addition to lung airway inflammation, T. gondii infection can suppress allergic responses at systemic level. These results open the possibility that this protozoan infection could modulate other allergic disorders such as atopic dermatitis or oral allergies. Understanding the mechanisms by which different microorganisms regulate inflammation may potentially lead to the development of strategies aimed to control atopic diseases. Fil: Fenoy, Ignacio Martín. Universidad Nacional de San Martín. Escuela de Ciencia y Tecnología. Centro de Estudios en Salud y Medio Ambiente; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Sánchez, Vanesa Roxana. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional de San Martín. Escuela de Ciencia y Tecnología. Centro de Estudios en Salud y Medio Ambiente; Argentina Fil: Soto, Ariadna Soledad. Universidad Nacional de San Martín. Escuela de Ciencia y Tecnología. Centro de Estudios en Salud y Medio Ambiente; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Picchio, Mariano Sergio. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional de San Martín. Escuela de Ciencia y Tecnología. Centro de Estudios en Salud y Medio Ambiente; Argentina Fil: Martín, Valentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional de San Martín. Escuela de Ciencia y Tecnología. Centro de Estudios en Salud y Medio Ambiente; Argentina Fil: Goldman, Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional de San Martín. Escuela de Ciencia y Tecnología. Centro de Estudios en Salud y Medio Ambiente; Argentina |
| description |
The increased prevalence of allergies in developed countries has been attributed to a reduced exposure to some microbes. In agreement with epidemiological studies, we previously showed that Toxoplasma gondii infection prevents allergic airway inflammation. The mechanisms would be related to the strong Th1 response induced by the parasite and to regulatory cell induction. Herein we further characterized whether T. gondii allergy modulation extents to a systemic level or if it is limited to the lung. Parasite infection before allergic sensitization resulted in a diminished Th2 cytokine response and, when sensitized during acute infection, an increased in TGF-β production was detected. Allergen specific T cell proliferation was also reduced. Sensitization during both acute and chronic phases of infection resulted in a decreased anaphylaxis reaction. Our results extend earlier work and show that, in addition to lung airway inflammation, T. gondii infection can suppress allergic responses at systemic level. These results open the possibility that this protozoan infection could modulate other allergic disorders such as atopic dermatitis or oral allergies. Understanding the mechanisms by which different microorganisms regulate inflammation may potentially lead to the development of strategies aimed to control atopic diseases. |
| publishDate |
2015 |
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2015-07 |
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http://hdl.handle.net/11336/98633 Fenoy, Ignacio Martín; Sánchez, Vanesa Roxana; Soto, Ariadna Soledad; Picchio, Mariano Sergio; Martín, Valentina; et al.; Toxoplasma gondii infection modulate systemic allergic immune response in BALB/c mice; Academic Press Inc Elsevier Science; Experimental Parasitology; 154; 7-2015; 47-50 0014-4894 CONICET Digital CONICET |
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Fenoy, Ignacio Martín; Sánchez, Vanesa Roxana; Soto, Ariadna Soledad; Picchio, Mariano Sergio; Martín, Valentina; et al.; Toxoplasma gondii infection modulate systemic allergic immune response in BALB/c mice; Academic Press Inc Elsevier Science; Experimental Parasitology; 154; 7-2015; 47-50 0014-4894 CONICET Digital CONICET |
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eng |
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