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
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/281908

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network_name_str CONICET Digital (CONICET)
spelling 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.
publishDate 2025
dc.date.none.fl_str_mv 2025-10
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info:eu-repo/semantics/publishedVersion
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info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv 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
url http://hdl.handle.net/11336/281908
identifier_str_mv 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
dc.language.none.fl_str_mv eng
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dc.publisher.none.fl_str_mv Frontiers Media
publisher.none.fl_str_mv Frontiers Media
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