Galectin-8 deficiency promotes chronic splenomegaly persistence in Chagas disease
- Autores
- Bertelli, Adriano; Saborit Badano, Juan Ignacio; Beccaria, Cristian Gabriel; Vanagas, Laura; Angel, Sergio Oscar; Campetella, Oscar Eduardo; Gruppi, Adriana; Leguizamon, Maria Susana
- Año de publicación
- 2025
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Galectins (Gals) are mammalian lectins with affinity for b-galactosides, whichdrive the immune response through several mechanisms. The specific role ofGal-8 in the development of inflammation remains controversial, as it has beenshown to induce either T cell proliferation or regulation in different models.During the acute phase of Trypanosoma cruzi infection, a characteristicsplenomegaly is induced that is associated with both antigen-specific andnon-specific polyclonal lymphocyte proliferation. This splenomegaly resolvesas the infection transitions to the chronic phase. While the pathogenesis ofChagas disease is not yet fully understood, it is widely accepted to involve bothparasite persistence and the host immune response. In this study, C57BL/6J andGal-8-deficient (KO) mice infected with the Ac strain were analyzed during thechronic phase (4 months post-infection). Notably, infected Gal-8KO mice failedto resolve the T. cruzi-induced acute phase splenomegaly. Despite this,parasitemia, spleen parasite load, and survival rates were comparable betweenthe two groups, suggesting that Gal-8 is not involved in parasite control. Theobserved differences in spleen cellularity were primarily attributed to Tlymphocyte proliferation, while B cells exhibited no significative changes intotal cell number, proliferation levels and production of total and parasitespecific antibodies. Overall, our results reveal that Gal-8 plays an antiinflammatory role during chronic T. cruzi infection and is critical in controllingsplenomegaly, a process for which no associated regulatory molecules havebeen identified to date.
Fil: Bertelli, Adriano. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas. - Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Biotecnológicas; Argentina
Fil: Saborit Badano, Juan Ignacio. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas. - Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Biotecnológicas; Argentina
Fil: Beccaria, Cristian Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Vanagas, Laura. Universidad Nacional de San Martin. Instituto Tecnologico de Chascomus. - Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnologico Conicet - la Plata. Instituto Tecnologico de Chascomus.; Argentina
Fil: Angel, Sergio Oscar. Universidad Nacional de San Martin. Instituto Tecnologico de Chascomus. - Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnologico Conicet - la Plata. Instituto Tecnologico de Chascomus.; Argentina
Fil: Campetella, Oscar Eduardo. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas. - Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Biotecnológicas; Argentina
Fil: Gruppi, Adriana. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Leguizamon, Maria Susana. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas. - Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Biotecnológicas; Argentina - Materia
-
CHAGAS DISEASE
GALECTIN-8 INFLAMMATION
SPLENOMEGALY
TRYPANOSOMA CRUZI - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
.jpg)
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/281908
Ver los metadatos del registro completo
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Galectin-8 deficiency promotes chronic splenomegaly persistence in Chagas diseaseBertelli, AdrianoSaborit Badano, Juan IgnacioBeccaria, Cristian GabrielVanagas, LauraAngel, Sergio OscarCampetella, Oscar EduardoGruppi, AdrianaLeguizamon, Maria SusanaCHAGAS DISEASEGALECTIN-8 INFLAMMATIONSPLENOMEGALYTRYPANOSOMA CRUZIhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Galectins (Gals) are mammalian lectins with affinity for b-galactosides, whichdrive the immune response through several mechanisms. The specific role ofGal-8 in the development of inflammation remains controversial, as it has beenshown to induce either T cell proliferation or regulation in different models.During the acute phase of Trypanosoma cruzi infection, a characteristicsplenomegaly is induced that is associated with both antigen-specific andnon-specific polyclonal lymphocyte proliferation. This splenomegaly resolvesas the infection transitions to the chronic phase. While the pathogenesis ofChagas disease is not yet fully understood, it is widely accepted to involve bothparasite persistence and the host immune response. In this study, C57BL/6J andGal-8-deficient (KO) mice infected with the Ac strain were analyzed during thechronic phase (4 months post-infection). Notably, infected Gal-8KO mice failedto resolve the T. cruzi-induced acute phase splenomegaly. Despite this,parasitemia, spleen parasite load, and survival rates were comparable betweenthe two groups, suggesting that Gal-8 is not involved in parasite control. Theobserved differences in spleen cellularity were primarily attributed to Tlymphocyte proliferation, while B cells exhibited no significative changes intotal cell number, proliferation levels and production of total and parasitespecific antibodies. Overall, our results reveal that Gal-8 plays an antiinflammatory role during chronic T. cruzi infection and is critical in controllingsplenomegaly, a process for which no associated regulatory molecules havebeen identified to date.Fil: Bertelli, Adriano. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas. - Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Biotecnológicas; ArgentinaFil: Saborit Badano, Juan Ignacio. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas. - Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Biotecnológicas; ArgentinaFil: Beccaria, Cristian Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Vanagas, Laura. Universidad Nacional de San Martin. Instituto Tecnologico de Chascomus. - Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnologico Conicet - la Plata. Instituto Tecnologico de Chascomus.; ArgentinaFil: Angel, Sergio Oscar. Universidad Nacional de San Martin. Instituto Tecnologico de Chascomus. - Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnologico Conicet - la Plata. Instituto Tecnologico de Chascomus.; ArgentinaFil: Campetella, Oscar Eduardo. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas. - Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Biotecnológicas; ArgentinaFil: Gruppi, Adriana. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Leguizamon, Maria Susana. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas. - Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Biotecnológicas; ArgentinaFrontiers Media2025-10info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/281908Bertelli, Adriano; Saborit Badano, Juan Ignacio; Beccaria, Cristian Gabriel; Vanagas, Laura; Angel, Sergio Oscar; et al.; Galectin-8 deficiency promotes chronic splenomegaly persistence in Chagas disease; Frontiers Media; Frontiers in Cellular and Infection Microbiology; 15; 10-2025; 1-162235-2988CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.frontiersin.org/articles/10.3389/fcimb.2025.1625938/fullinfo:eu-repo/semantics/altIdentifier/doi/10.3389/fcimb.2025.1625938info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2026-03-31T15:07:28Zoai:ri.conicet.gov.ar:11336/281908instacron: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:34982026-03-31 15:07:28.303CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
| dc.title.none.fl_str_mv |
Galectin-8 deficiency promotes chronic splenomegaly persistence in Chagas disease |
| title |
Galectin-8 deficiency promotes chronic splenomegaly persistence in Chagas disease |
| spellingShingle |
Galectin-8 deficiency promotes chronic splenomegaly persistence in Chagas disease Bertelli, Adriano CHAGAS DISEASE GALECTIN-8 INFLAMMATION SPLENOMEGALY TRYPANOSOMA CRUZI |
| title_short |
Galectin-8 deficiency promotes chronic splenomegaly persistence in Chagas disease |
| title_full |
Galectin-8 deficiency promotes chronic splenomegaly persistence in Chagas disease |
| title_fullStr |
Galectin-8 deficiency promotes chronic splenomegaly persistence in Chagas disease |
| title_full_unstemmed |
Galectin-8 deficiency promotes chronic splenomegaly persistence in Chagas disease |
| title_sort |
Galectin-8 deficiency promotes chronic splenomegaly persistence in Chagas disease |
| dc.creator.none.fl_str_mv |
Bertelli, Adriano Saborit Badano, Juan Ignacio Beccaria, Cristian Gabriel Vanagas, Laura Angel, Sergio Oscar Campetella, Oscar Eduardo Gruppi, Adriana Leguizamon, Maria Susana |
| author |
Bertelli, Adriano |
| author_facet |
Bertelli, Adriano Saborit Badano, Juan Ignacio Beccaria, Cristian Gabriel Vanagas, Laura Angel, Sergio Oscar Campetella, Oscar Eduardo Gruppi, Adriana Leguizamon, Maria Susana |
| author_role |
author |
| author2 |
Saborit Badano, Juan Ignacio Beccaria, Cristian Gabriel Vanagas, Laura Angel, Sergio Oscar Campetella, Oscar Eduardo Gruppi, Adriana Leguizamon, Maria Susana |
| author2_role |
author author author author author author author |
| dc.subject.none.fl_str_mv |
CHAGAS DISEASE GALECTIN-8 INFLAMMATION SPLENOMEGALY TRYPANOSOMA CRUZI |
| topic |
CHAGAS DISEASE GALECTIN-8 INFLAMMATION SPLENOMEGALY TRYPANOSOMA CRUZI |
| purl_subject.fl_str_mv |
https://purl.org/becyt/ford/1.6 https://purl.org/becyt/ford/1 |
| dc.description.none.fl_txt_mv |
Galectins (Gals) are mammalian lectins with affinity for b-galactosides, whichdrive the immune response through several mechanisms. The specific role ofGal-8 in the development of inflammation remains controversial, as it has beenshown to induce either T cell proliferation or regulation in different models.During the acute phase of Trypanosoma cruzi infection, a characteristicsplenomegaly is induced that is associated with both antigen-specific andnon-specific polyclonal lymphocyte proliferation. This splenomegaly resolvesas the infection transitions to the chronic phase. While the pathogenesis ofChagas disease is not yet fully understood, it is widely accepted to involve bothparasite persistence and the host immune response. In this study, C57BL/6J andGal-8-deficient (KO) mice infected with the Ac strain were analyzed during thechronic phase (4 months post-infection). Notably, infected Gal-8KO mice failedto resolve the T. cruzi-induced acute phase splenomegaly. Despite this,parasitemia, spleen parasite load, and survival rates were comparable betweenthe two groups, suggesting that Gal-8 is not involved in parasite control. Theobserved differences in spleen cellularity were primarily attributed to Tlymphocyte proliferation, while B cells exhibited no significative changes intotal cell number, proliferation levels and production of total and parasitespecific antibodies. Overall, our results reveal that Gal-8 plays an antiinflammatory role during chronic T. cruzi infection and is critical in controllingsplenomegaly, a process for which no associated regulatory molecules havebeen identified to date. Fil: Bertelli, Adriano. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas. - Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Biotecnológicas; Argentina Fil: Saborit Badano, Juan Ignacio. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas. - Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Biotecnológicas; Argentina Fil: Beccaria, Cristian Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina Fil: Vanagas, Laura. Universidad Nacional de San Martin. Instituto Tecnologico de Chascomus. - Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnologico Conicet - la Plata. Instituto Tecnologico de Chascomus.; Argentina Fil: Angel, Sergio Oscar. Universidad Nacional de San Martin. Instituto Tecnologico de Chascomus. - Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnologico Conicet - la Plata. Instituto Tecnologico de Chascomus.; Argentina Fil: Campetella, Oscar Eduardo. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas. - Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Biotecnológicas; Argentina Fil: Gruppi, Adriana. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina Fil: Leguizamon, Maria Susana. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas. - Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Biotecnológicas; Argentina |
| description |
Galectins (Gals) are mammalian lectins with affinity for b-galactosides, whichdrive the immune response through several mechanisms. The specific role ofGal-8 in the development of inflammation remains controversial, as it has beenshown to induce either T cell proliferation or regulation in different models.During the acute phase of Trypanosoma cruzi infection, a characteristicsplenomegaly is induced that is associated with both antigen-specific andnon-specific polyclonal lymphocyte proliferation. This splenomegaly resolvesas the infection transitions to the chronic phase. While the pathogenesis ofChagas disease is not yet fully understood, it is widely accepted to involve bothparasite persistence and the host immune response. In this study, C57BL/6J andGal-8-deficient (KO) mice infected with the Ac strain were analyzed during thechronic phase (4 months post-infection). Notably, infected Gal-8KO mice failedto resolve the T. cruzi-induced acute phase splenomegaly. Despite this,parasitemia, spleen parasite load, and survival rates were comparable betweenthe two groups, suggesting that Gal-8 is not involved in parasite control. Theobserved differences in spleen cellularity were primarily attributed to Tlymphocyte proliferation, while B cells exhibited no significative changes intotal cell number, proliferation levels and production of total and parasitespecific antibodies. Overall, our results reveal that Gal-8 plays an antiinflammatory role during chronic T. cruzi infection and is critical in controllingsplenomegaly, a process for which no associated regulatory molecules havebeen identified to date. |
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2025 |
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2025-10 |
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http://hdl.handle.net/11336/281908 Bertelli, Adriano; Saborit Badano, Juan Ignacio; Beccaria, Cristian Gabriel; Vanagas, Laura; Angel, Sergio Oscar; et al.; Galectin-8 deficiency promotes chronic splenomegaly persistence in Chagas disease; Frontiers Media; Frontiers in Cellular and Infection Microbiology; 15; 10-2025; 1-16 2235-2988 CONICET Digital CONICET |
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http://hdl.handle.net/11336/281908 |
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Bertelli, Adriano; Saborit Badano, Juan Ignacio; Beccaria, Cristian Gabriel; Vanagas, Laura; Angel, Sergio Oscar; et al.; Galectin-8 deficiency promotes chronic splenomegaly persistence in Chagas disease; Frontiers Media; Frontiers in Cellular and Infection Microbiology; 15; 10-2025; 1-16 2235-2988 CONICET Digital CONICET |
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