Proposed model: Mechanisms of immunomodulation induced by probiotic bacteria

Autores
Maldonado Galdeano, María Carolina; de Moreno, Maria Alejandra; Vinderola, Celso Gabriel; Bibas Bonet, María Eugenia; Perdigon, Gabriela del Valle
Año de publicación
2007
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
The mammalian microbiota comprises several hundred different bacterial species, many of which have a beneficial effect on the host. For example, they are involved in preventing colonization of the gut by pathogens and maintaining the gut mucosal immunity (85). The gut microbiota is more abundant in the large intestine of mammals, with densities rising to over 1011 organisms/g intestinal content (84, 86). The number of bacterial cells in the entire gut exceeds the number of eukaryotic cells in the host, but under normal circumstance they coexist without any adverse effect on the host. The influence of the resident microflora on mucosal immune function and gut health has become an area of scientific and clinical importance (22, 26). There is an active dialogue between the commensal microorganisms and the host mucosal immune system (21, 48). This cross talk elicits different host responses to commensal and pathogenic bacteria. Commensal bacteria may even share molecular patterns recognized by toll-like receptors (TLRs), which can recognize patterns associated mainly with pathogens. However, the mucosal immune system of the healthy intestine allows the persistence of this microbiota associated with the intestine and avoids immunological tolerance, maintaining the intestinal homeostasis. Now, there is acceptance of the concept that oral tolerance is not generated by commensal intestinal bacteria; the host would ignore or fail to recognize the presence of indigenous microorganisms (49). The healthy host is able to elicit a good mucosal immune response against luminal antigens and to maintain a “physiological state of inflammation” in the gut, but it is also capable of responding to invading commensal organisms or pathogens. In the healthy host the penetration of the commensal bacteria is usually prevented by the barrier afforded by the intestinal epithelium and the immune cells associated with the mucosa, which are highly adapted to the presence of the normal microbiota (71). The signals sent by these microorganisms prevent their penetration and keep them outside the intestinal tissue. If the commensal microorganisms invade the host tissues, the innate immune mechanisms contribute to their rapid clearance, but when pathogens enter the intestine, innate and adaptive mechanisms are coordinately stimulated to respond to the danger signals (38, 60). Although mucosal epithelial tissues form an efficient barrier that prevents the entrance of the environmental pathogens and the external antigens into the host internal milieu, mucosal tissues represent the main sites of infection by pathogens. Many attempts have been made to understand the gut immunomodulation by pathogenic bacteria but not the mechanisms involved in the modulation of the gut immune system by commensal bacteria and by nonpathogenic microorganisms present in many foods included in the daily diet.
Fil: Maldonado Galdeano, María Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Centro de Referencia para Lactobacilos; Argentina. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; Argentina
Fil: de Moreno, Maria Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Centro de Referencia para Lactobacilos; Argentina. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; Argentina
Fil: Vinderola, Celso Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Centro de Referencia para Lactobacilos; Argentina
Fil: Bibas Bonet, María Eugenia. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; Argentina
Fil: Perdigon, Gabriela del Valle. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Centro de Referencia para Lactobacilos; Argentina. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; Argentina
Materia
Immunomodulation
Probiotic
Immune Mechanisms
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:11336/53752

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spelling Proposed model: Mechanisms of immunomodulation induced by probiotic bacteriaMaldonado Galdeano, María Carolinade Moreno, Maria AlejandraVinderola, Celso GabrielBibas Bonet, María EugeniaPerdigon, Gabriela del ValleImmunomodulationProbioticImmune Mechanismshttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3The mammalian microbiota comprises several hundred different bacterial species, many of which have a beneficial effect on the host. For example, they are involved in preventing colonization of the gut by pathogens and maintaining the gut mucosal immunity (85). The gut microbiota is more abundant in the large intestine of mammals, with densities rising to over 1011 organisms/g intestinal content (84, 86). The number of bacterial cells in the entire gut exceeds the number of eukaryotic cells in the host, but under normal circumstance they coexist without any adverse effect on the host. The influence of the resident microflora on mucosal immune function and gut health has become an area of scientific and clinical importance (22, 26). There is an active dialogue between the commensal microorganisms and the host mucosal immune system (21, 48). This cross talk elicits different host responses to commensal and pathogenic bacteria. Commensal bacteria may even share molecular patterns recognized by toll-like receptors (TLRs), which can recognize patterns associated mainly with pathogens. However, the mucosal immune system of the healthy intestine allows the persistence of this microbiota associated with the intestine and avoids immunological tolerance, maintaining the intestinal homeostasis. Now, there is acceptance of the concept that oral tolerance is not generated by commensal intestinal bacteria; the host would ignore or fail to recognize the presence of indigenous microorganisms (49). The healthy host is able to elicit a good mucosal immune response against luminal antigens and to maintain a “physiological state of inflammation” in the gut, but it is also capable of responding to invading commensal organisms or pathogens. In the healthy host the penetration of the commensal bacteria is usually prevented by the barrier afforded by the intestinal epithelium and the immune cells associated with the mucosa, which are highly adapted to the presence of the normal microbiota (71). The signals sent by these microorganisms prevent their penetration and keep them outside the intestinal tissue. If the commensal microorganisms invade the host tissues, the innate immune mechanisms contribute to their rapid clearance, but when pathogens enter the intestine, innate and adaptive mechanisms are coordinately stimulated to respond to the danger signals (38, 60). Although mucosal epithelial tissues form an efficient barrier that prevents the entrance of the environmental pathogens and the external antigens into the host internal milieu, mucosal tissues represent the main sites of infection by pathogens. Many attempts have been made to understand the gut immunomodulation by pathogenic bacteria but not the mechanisms involved in the modulation of the gut immune system by commensal bacteria and by nonpathogenic microorganisms present in many foods included in the daily diet.Fil: Maldonado Galdeano, María Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Centro de Referencia para Lactobacilos; Argentina. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; ArgentinaFil: de Moreno, Maria Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Centro de Referencia para Lactobacilos; Argentina. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; ArgentinaFil: Vinderola, Celso Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Centro de Referencia para Lactobacilos; ArgentinaFil: Bibas Bonet, María Eugenia. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; ArgentinaFil: Perdigon, Gabriela del Valle. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Centro de Referencia para Lactobacilos; Argentina. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; ArgentinaAmerican Society for Microbiology2007-05-12info: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/11336/53752Maldonado Galdeano, María Carolina; de Moreno, Maria Alejandra; Vinderola, Celso Gabriel; Bibas Bonet, María Eugenia; Perdigon, Gabriela del Valle; Proposed model: Mechanisms of immunomodulation induced by probiotic bacteria; American Society for Microbiology; Clinical and Vaccine Immunology; 14; 5; 12-5-2007; 485-4921556-68111556-679XCONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1128/CVI.00406-06info:eu-repo/semantics/altIdentifier/url/http://cvi.asm.org/content/14/5/485info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1865623/info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:05:56Zoai:ri.conicet.gov.ar:11336/53752instacron: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:34982025-09-29 10:05:57.163CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Proposed model: Mechanisms of immunomodulation induced by probiotic bacteria
title Proposed model: Mechanisms of immunomodulation induced by probiotic bacteria
spellingShingle Proposed model: Mechanisms of immunomodulation induced by probiotic bacteria
Maldonado Galdeano, María Carolina
Immunomodulation
Probiotic
Immune Mechanisms
title_short Proposed model: Mechanisms of immunomodulation induced by probiotic bacteria
title_full Proposed model: Mechanisms of immunomodulation induced by probiotic bacteria
title_fullStr Proposed model: Mechanisms of immunomodulation induced by probiotic bacteria
title_full_unstemmed Proposed model: Mechanisms of immunomodulation induced by probiotic bacteria
title_sort Proposed model: Mechanisms of immunomodulation induced by probiotic bacteria
dc.creator.none.fl_str_mv Maldonado Galdeano, María Carolina
de Moreno, Maria Alejandra
Vinderola, Celso Gabriel
Bibas Bonet, María Eugenia
Perdigon, Gabriela del Valle
author Maldonado Galdeano, María Carolina
author_facet Maldonado Galdeano, María Carolina
de Moreno, Maria Alejandra
Vinderola, Celso Gabriel
Bibas Bonet, María Eugenia
Perdigon, Gabriela del Valle
author_role author
author2 de Moreno, Maria Alejandra
Vinderola, Celso Gabriel
Bibas Bonet, María Eugenia
Perdigon, Gabriela del Valle
author2_role author
author
author
author
dc.subject.none.fl_str_mv Immunomodulation
Probiotic
Immune Mechanisms
topic Immunomodulation
Probiotic
Immune Mechanisms
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 mammalian microbiota comprises several hundred different bacterial species, many of which have a beneficial effect on the host. For example, they are involved in preventing colonization of the gut by pathogens and maintaining the gut mucosal immunity (85). The gut microbiota is more abundant in the large intestine of mammals, with densities rising to over 1011 organisms/g intestinal content (84, 86). The number of bacterial cells in the entire gut exceeds the number of eukaryotic cells in the host, but under normal circumstance they coexist without any adverse effect on the host. The influence of the resident microflora on mucosal immune function and gut health has become an area of scientific and clinical importance (22, 26). There is an active dialogue between the commensal microorganisms and the host mucosal immune system (21, 48). This cross talk elicits different host responses to commensal and pathogenic bacteria. Commensal bacteria may even share molecular patterns recognized by toll-like receptors (TLRs), which can recognize patterns associated mainly with pathogens. However, the mucosal immune system of the healthy intestine allows the persistence of this microbiota associated with the intestine and avoids immunological tolerance, maintaining the intestinal homeostasis. Now, there is acceptance of the concept that oral tolerance is not generated by commensal intestinal bacteria; the host would ignore or fail to recognize the presence of indigenous microorganisms (49). The healthy host is able to elicit a good mucosal immune response against luminal antigens and to maintain a “physiological state of inflammation” in the gut, but it is also capable of responding to invading commensal organisms or pathogens. In the healthy host the penetration of the commensal bacteria is usually prevented by the barrier afforded by the intestinal epithelium and the immune cells associated with the mucosa, which are highly adapted to the presence of the normal microbiota (71). The signals sent by these microorganisms prevent their penetration and keep them outside the intestinal tissue. If the commensal microorganisms invade the host tissues, the innate immune mechanisms contribute to their rapid clearance, but when pathogens enter the intestine, innate and adaptive mechanisms are coordinately stimulated to respond to the danger signals (38, 60). Although mucosal epithelial tissues form an efficient barrier that prevents the entrance of the environmental pathogens and the external antigens into the host internal milieu, mucosal tissues represent the main sites of infection by pathogens. Many attempts have been made to understand the gut immunomodulation by pathogenic bacteria but not the mechanisms involved in the modulation of the gut immune system by commensal bacteria and by nonpathogenic microorganisms present in many foods included in the daily diet.
Fil: Maldonado Galdeano, María Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Centro de Referencia para Lactobacilos; Argentina. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; Argentina
Fil: de Moreno, Maria Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Centro de Referencia para Lactobacilos; Argentina. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; Argentina
Fil: Vinderola, Celso Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Centro de Referencia para Lactobacilos; Argentina
Fil: Bibas Bonet, María Eugenia. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; Argentina
Fil: Perdigon, Gabriela del Valle. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Centro de Referencia para Lactobacilos; Argentina. Universidad Nacional de Tucumán. Facultad de Bioquímica, Química y Farmacia; Argentina
description The mammalian microbiota comprises several hundred different bacterial species, many of which have a beneficial effect on the host. For example, they are involved in preventing colonization of the gut by pathogens and maintaining the gut mucosal immunity (85). The gut microbiota is more abundant in the large intestine of mammals, with densities rising to over 1011 organisms/g intestinal content (84, 86). The number of bacterial cells in the entire gut exceeds the number of eukaryotic cells in the host, but under normal circumstance they coexist without any adverse effect on the host. The influence of the resident microflora on mucosal immune function and gut health has become an area of scientific and clinical importance (22, 26). There is an active dialogue between the commensal microorganisms and the host mucosal immune system (21, 48). This cross talk elicits different host responses to commensal and pathogenic bacteria. Commensal bacteria may even share molecular patterns recognized by toll-like receptors (TLRs), which can recognize patterns associated mainly with pathogens. However, the mucosal immune system of the healthy intestine allows the persistence of this microbiota associated with the intestine and avoids immunological tolerance, maintaining the intestinal homeostasis. Now, there is acceptance of the concept that oral tolerance is not generated by commensal intestinal bacteria; the host would ignore or fail to recognize the presence of indigenous microorganisms (49). The healthy host is able to elicit a good mucosal immune response against luminal antigens and to maintain a “physiological state of inflammation” in the gut, but it is also capable of responding to invading commensal organisms or pathogens. In the healthy host the penetration of the commensal bacteria is usually prevented by the barrier afforded by the intestinal epithelium and the immune cells associated with the mucosa, which are highly adapted to the presence of the normal microbiota (71). The signals sent by these microorganisms prevent their penetration and keep them outside the intestinal tissue. If the commensal microorganisms invade the host tissues, the innate immune mechanisms contribute to their rapid clearance, but when pathogens enter the intestine, innate and adaptive mechanisms are coordinately stimulated to respond to the danger signals (38, 60). Although mucosal epithelial tissues form an efficient barrier that prevents the entrance of the environmental pathogens and the external antigens into the host internal milieu, mucosal tissues represent the main sites of infection by pathogens. Many attempts have been made to understand the gut immunomodulation by pathogenic bacteria but not the mechanisms involved in the modulation of the gut immune system by commensal bacteria and by nonpathogenic microorganisms present in many foods included in the daily diet.
publishDate 2007
dc.date.none.fl_str_mv 2007-05-12
dc.type.none.fl_str_mv info:eu-repo/semantics/article
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/11336/53752
Maldonado Galdeano, María Carolina; de Moreno, Maria Alejandra; Vinderola, Celso Gabriel; Bibas Bonet, María Eugenia; Perdigon, Gabriela del Valle; Proposed model: Mechanisms of immunomodulation induced by probiotic bacteria; American Society for Microbiology; Clinical and Vaccine Immunology; 14; 5; 12-5-2007; 485-492
1556-6811
1556-679X
CONICET Digital
CONICET
url http://hdl.handle.net/11336/53752
identifier_str_mv Maldonado Galdeano, María Carolina; de Moreno, Maria Alejandra; Vinderola, Celso Gabriel; Bibas Bonet, María Eugenia; Perdigon, Gabriela del Valle; Proposed model: Mechanisms of immunomodulation induced by probiotic bacteria; American Society for Microbiology; Clinical and Vaccine Immunology; 14; 5; 12-5-2007; 485-492
1556-6811
1556-679X
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1128/CVI.00406-06
info:eu-repo/semantics/altIdentifier/url/http://cvi.asm.org/content/14/5/485
info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1865623/
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
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dc.format.none.fl_str_mv application/pdf
application/pdf
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dc.publisher.none.fl_str_mv American Society for Microbiology
publisher.none.fl_str_mv American Society for Microbiology
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repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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