B. lactis INL1 improves macrophage immune function and modulates events associated with colorectal cancer cell aggressiveness

Autores
Carriere, Pedro Matias; Novoa Díaz, María Belén; Birkenstok, Cintia Noelia; Picardi, Gonzalo; Sica, Gabriela; Calvo, Natalia Graciela; Vinderola, Celso Gabriel; Gentili, Claudia Rosana
Año de publicación
2024
Idioma
inglés
Tipo de recurso
documento de conferencia
Estado
versión publicada
Descripción
The human milk-derived strain Bifidobacterium animalis subsp. lactis INL1 (B. lactis INL1) (agreement UNS-UNL N°REC-1092496-2) displays properties of a novel probiotic. Previously we showed that in colorectal cancer (CRC) cells, certain probiotics modulate gene expression associated with macrophage activity and that B. lactis INL1 improves macrophage physiology under lipopolysaccharide (LPS) action. Herein we investigate if B. lactis INL1 is able to modulate: 1- the macrophage activity in an inflammatory context and 2- the interaction between macrophages and CRC cells (which are under a pro-tumor factor action). We observed that pretreatment with 5% of cell-free supernatant (CFS) from B. lactis INL1 for 3 h (condition that not affect cell viability) enhances the migratory and phagocytic capacity of RAW264.7 macrophages promoted by LPS exposure for 24 h. Previously we showed that parathyroid hormone-related peptide (PTHrP) is a pro-tumor factor that favors HCT116 cells aggressiveness via E-cadherin deregulation. Also, our in silico analysis revealed that the macrophage inhibitory cytokine GDF15 is overexpressed in HCT116 cells. In view of these findings, we next proceeded to evaluate the expression of both markers. Western blot analysis revealed that the pre-treatment of HCT116 cells with CFS from B. lactis INL1 followed by PTHrP exposition for 24 h reverses the changes in E-cadherin and GDF15 expression induced by PTHrP. Finally, we evaluated whether the conditioned medium from HCT116 cells pre-treated with B. lactis INL1 CFS (MCT-T) and exposed to PTHrP affects macrophage function. Using a viability assay, we observed that MCT-T enhanced macrophage viability compared to conditioned medium from cells under PTHrP action but untreated with probiotic. These results suggest that expression and secretion of GDF15 from tumor cells may mediate the suppressive effects of tumor conditioned medium on immune cells, and that B. lactis INL1 could modulate this process.
Fil: Carriere, Pedro Matias. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina
Fil: Novoa Díaz, María Belén. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina
Fil: Birkenstok, Cintia Noelia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina
Fil: Picardi, Gonzalo. Universidad Nacional del Sur. Departamento de Ciencias de la Salud; Argentina
Fil: Sica, Gabriela. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Universidad Nacional del Sur. Departamento de Ciencias de la Salud; Argentina
Fil: Calvo, Natalia Graciela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina
Fil: Vinderola, Celso Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe. Instituto de Lactología Industrial. Universidad Nacional del Litoral. Facultad de Ingeniería Química. Instituto de Lactología Industrial; Argentina
Fil: Gentili, Claudia Rosana. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina
LXIX Reunión Anual de la Sociedad Argentina de Investigación Clínica y XXVI Sociedad Argentina de Fisiología
Ciudad Autónoma de Buenos Aires
Argentina
Sociedad Argentina de Investigación Clínica
Sociedad Argentina de Fisiología
Asociación Latinoamericana de Ciencias Fisiológicas
Materia
B. LACTIS INL1
MACROPHAGES
COLORECTAL CANCER
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:11336/264234

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network_name_str CONICET Digital (CONICET)
spelling B. lactis INL1 improves macrophage immune function and modulates events associated with colorectal cancer cell aggressivenessCarriere, Pedro MatiasNovoa Díaz, María BelénBirkenstok, Cintia NoeliaPicardi, GonzaloSica, GabrielaCalvo, Natalia GracielaVinderola, Celso GabrielGentili, Claudia RosanaB. LACTIS INL1MACROPHAGESCOLORECTAL CANCERhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1The human milk-derived strain Bifidobacterium animalis subsp. lactis INL1 (B. lactis INL1) (agreement UNS-UNL N°REC-1092496-2) displays properties of a novel probiotic. Previously we showed that in colorectal cancer (CRC) cells, certain probiotics modulate gene expression associated with macrophage activity and that B. lactis INL1 improves macrophage physiology under lipopolysaccharide (LPS) action. Herein we investigate if B. lactis INL1 is able to modulate: 1- the macrophage activity in an inflammatory context and 2- the interaction between macrophages and CRC cells (which are under a pro-tumor factor action). We observed that pretreatment with 5% of cell-free supernatant (CFS) from B. lactis INL1 for 3 h (condition that not affect cell viability) enhances the migratory and phagocytic capacity of RAW264.7 macrophages promoted by LPS exposure for 24 h. Previously we showed that parathyroid hormone-related peptide (PTHrP) is a pro-tumor factor that favors HCT116 cells aggressiveness via E-cadherin deregulation. Also, our in silico analysis revealed that the macrophage inhibitory cytokine GDF15 is overexpressed in HCT116 cells. In view of these findings, we next proceeded to evaluate the expression of both markers. Western blot analysis revealed that the pre-treatment of HCT116 cells with CFS from B. lactis INL1 followed by PTHrP exposition for 24 h reverses the changes in E-cadherin and GDF15 expression induced by PTHrP. Finally, we evaluated whether the conditioned medium from HCT116 cells pre-treated with B. lactis INL1 CFS (MCT-T) and exposed to PTHrP affects macrophage function. Using a viability assay, we observed that MCT-T enhanced macrophage viability compared to conditioned medium from cells under PTHrP action but untreated with probiotic. These results suggest that expression and secretion of GDF15 from tumor cells may mediate the suppressive effects of tumor conditioned medium on immune cells, and that B. lactis INL1 could modulate this process.Fil: Carriere, Pedro Matias. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; ArgentinaFil: Novoa Díaz, María Belén. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; ArgentinaFil: Birkenstok, Cintia Noelia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; ArgentinaFil: Picardi, Gonzalo. Universidad Nacional del Sur. Departamento de Ciencias de la Salud; ArgentinaFil: Sica, Gabriela. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Universidad Nacional del Sur. Departamento de Ciencias de la Salud; ArgentinaFil: Calvo, Natalia Graciela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; ArgentinaFil: Vinderola, Celso Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe. Instituto de Lactología Industrial. Universidad Nacional del Litoral. Facultad de Ingeniería Química. Instituto de Lactología Industrial; ArgentinaFil: Gentili, Claudia Rosana. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; ArgentinaLXIX Reunión Anual de la Sociedad Argentina de Investigación Clínica y XXVI Sociedad Argentina de FisiologíaCiudad Autónoma de Buenos AiresArgentinaSociedad Argentina de Investigación ClínicaSociedad Argentina de FisiologíaAsociación Latinoamericana de Ciencias FisiológicasFundación Revista MedicinaRey, Rodolfo2024info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectReuniónJournalhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/264234B. lactis INL1 improves macrophage immune function and modulates events associated with colorectal cancer cell aggressiveness; LXIX Reunión Anual de la Sociedad Argentina de Investigación Clínica y XXVI Sociedad Argentina de Fisiología; Ciudad Autónoma de Buenos Aires; Argentina; 2024; 165 - 1651669-9106CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.medicinabuenosaires.com/indices-de-2020/Internacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-15T15:11:28Zoai:ri.conicet.gov.ar:11336/264234instacron: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:34982025-10-15 15:11:28.848CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv B. lactis INL1 improves macrophage immune function and modulates events associated with colorectal cancer cell aggressiveness
title B. lactis INL1 improves macrophage immune function and modulates events associated with colorectal cancer cell aggressiveness
spellingShingle B. lactis INL1 improves macrophage immune function and modulates events associated with colorectal cancer cell aggressiveness
Carriere, Pedro Matias
B. LACTIS INL1
MACROPHAGES
COLORECTAL CANCER
title_short B. lactis INL1 improves macrophage immune function and modulates events associated with colorectal cancer cell aggressiveness
title_full B. lactis INL1 improves macrophage immune function and modulates events associated with colorectal cancer cell aggressiveness
title_fullStr B. lactis INL1 improves macrophage immune function and modulates events associated with colorectal cancer cell aggressiveness
title_full_unstemmed B. lactis INL1 improves macrophage immune function and modulates events associated with colorectal cancer cell aggressiveness
title_sort B. lactis INL1 improves macrophage immune function and modulates events associated with colorectal cancer cell aggressiveness
dc.creator.none.fl_str_mv Carriere, Pedro Matias
Novoa Díaz, María Belén
Birkenstok, Cintia Noelia
Picardi, Gonzalo
Sica, Gabriela
Calvo, Natalia Graciela
Vinderola, Celso Gabriel
Gentili, Claudia Rosana
author Carriere, Pedro Matias
author_facet Carriere, Pedro Matias
Novoa Díaz, María Belén
Birkenstok, Cintia Noelia
Picardi, Gonzalo
Sica, Gabriela
Calvo, Natalia Graciela
Vinderola, Celso Gabriel
Gentili, Claudia Rosana
author_role author
author2 Novoa Díaz, María Belén
Birkenstok, Cintia Noelia
Picardi, Gonzalo
Sica, Gabriela
Calvo, Natalia Graciela
Vinderola, Celso Gabriel
Gentili, Claudia Rosana
author2_role author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Rey, Rodolfo
dc.subject.none.fl_str_mv B. LACTIS INL1
MACROPHAGES
COLORECTAL CANCER
topic B. LACTIS INL1
MACROPHAGES
COLORECTAL CANCER
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv The human milk-derived strain Bifidobacterium animalis subsp. lactis INL1 (B. lactis INL1) (agreement UNS-UNL N°REC-1092496-2) displays properties of a novel probiotic. Previously we showed that in colorectal cancer (CRC) cells, certain probiotics modulate gene expression associated with macrophage activity and that B. lactis INL1 improves macrophage physiology under lipopolysaccharide (LPS) action. Herein we investigate if B. lactis INL1 is able to modulate: 1- the macrophage activity in an inflammatory context and 2- the interaction between macrophages and CRC cells (which are under a pro-tumor factor action). We observed that pretreatment with 5% of cell-free supernatant (CFS) from B. lactis INL1 for 3 h (condition that not affect cell viability) enhances the migratory and phagocytic capacity of RAW264.7 macrophages promoted by LPS exposure for 24 h. Previously we showed that parathyroid hormone-related peptide (PTHrP) is a pro-tumor factor that favors HCT116 cells aggressiveness via E-cadherin deregulation. Also, our in silico analysis revealed that the macrophage inhibitory cytokine GDF15 is overexpressed in HCT116 cells. In view of these findings, we next proceeded to evaluate the expression of both markers. Western blot analysis revealed that the pre-treatment of HCT116 cells with CFS from B. lactis INL1 followed by PTHrP exposition for 24 h reverses the changes in E-cadherin and GDF15 expression induced by PTHrP. Finally, we evaluated whether the conditioned medium from HCT116 cells pre-treated with B. lactis INL1 CFS (MCT-T) and exposed to PTHrP affects macrophage function. Using a viability assay, we observed that MCT-T enhanced macrophage viability compared to conditioned medium from cells under PTHrP action but untreated with probiotic. These results suggest that expression and secretion of GDF15 from tumor cells may mediate the suppressive effects of tumor conditioned medium on immune cells, and that B. lactis INL1 could modulate this process.
Fil: Carriere, Pedro Matias. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina
Fil: Novoa Díaz, María Belén. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina
Fil: Birkenstok, Cintia Noelia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina
Fil: Picardi, Gonzalo. Universidad Nacional del Sur. Departamento de Ciencias de la Salud; Argentina
Fil: Sica, Gabriela. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Universidad Nacional del Sur. Departamento de Ciencias de la Salud; Argentina
Fil: Calvo, Natalia Graciela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina
Fil: Vinderola, Celso Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe. Instituto de Lactología Industrial. Universidad Nacional del Litoral. Facultad de Ingeniería Química. Instituto de Lactología Industrial; Argentina
Fil: Gentili, Claudia Rosana. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina
LXIX Reunión Anual de la Sociedad Argentina de Investigación Clínica y XXVI Sociedad Argentina de Fisiología
Ciudad Autónoma de Buenos Aires
Argentina
Sociedad Argentina de Investigación Clínica
Sociedad Argentina de Fisiología
Asociación Latinoamericana de Ciencias Fisiológicas
description The human milk-derived strain Bifidobacterium animalis subsp. lactis INL1 (B. lactis INL1) (agreement UNS-UNL N°REC-1092496-2) displays properties of a novel probiotic. Previously we showed that in colorectal cancer (CRC) cells, certain probiotics modulate gene expression associated with macrophage activity and that B. lactis INL1 improves macrophage physiology under lipopolysaccharide (LPS) action. Herein we investigate if B. lactis INL1 is able to modulate: 1- the macrophage activity in an inflammatory context and 2- the interaction between macrophages and CRC cells (which are under a pro-tumor factor action). We observed that pretreatment with 5% of cell-free supernatant (CFS) from B. lactis INL1 for 3 h (condition that not affect cell viability) enhances the migratory and phagocytic capacity of RAW264.7 macrophages promoted by LPS exposure for 24 h. Previously we showed that parathyroid hormone-related peptide (PTHrP) is a pro-tumor factor that favors HCT116 cells aggressiveness via E-cadherin deregulation. Also, our in silico analysis revealed that the macrophage inhibitory cytokine GDF15 is overexpressed in HCT116 cells. In view of these findings, we next proceeded to evaluate the expression of both markers. Western blot analysis revealed that the pre-treatment of HCT116 cells with CFS from B. lactis INL1 followed by PTHrP exposition for 24 h reverses the changes in E-cadherin and GDF15 expression induced by PTHrP. Finally, we evaluated whether the conditioned medium from HCT116 cells pre-treated with B. lactis INL1 CFS (MCT-T) and exposed to PTHrP affects macrophage function. Using a viability assay, we observed that MCT-T enhanced macrophage viability compared to conditioned medium from cells under PTHrP action but untreated with probiotic. These results suggest that expression and secretion of GDF15 from tumor cells may mediate the suppressive effects of tumor conditioned medium on immune cells, and that B. lactis INL1 could modulate this process.
publishDate 2024
dc.date.none.fl_str_mv 2024
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dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/264234
B. lactis INL1 improves macrophage immune function and modulates events associated with colorectal cancer cell aggressiveness; LXIX Reunión Anual de la Sociedad Argentina de Investigación Clínica y XXVI Sociedad Argentina de Fisiología; Ciudad Autónoma de Buenos Aires; Argentina; 2024; 165 - 165
1669-9106
CONICET Digital
CONICET
url http://hdl.handle.net/11336/264234
identifier_str_mv B. lactis INL1 improves macrophage immune function and modulates events associated with colorectal cancer cell aggressiveness; LXIX Reunión Anual de la Sociedad Argentina de Investigación Clínica y XXVI Sociedad Argentina de Fisiología; Ciudad Autónoma de Buenos Aires; Argentina; 2024; 165 - 165
1669-9106
CONICET Digital
CONICET
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dc.coverage.none.fl_str_mv Internacional
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publisher.none.fl_str_mv Fundación Revista Medicina
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