Elevated cyclic AMP inhibits mycobacterium tuberculosis-stimulated T-cell IFN-γ secretion through type I protein kinase A

Autores
Chung, Yoon-tae; Pasquinelli, Virginia; Jurado, Javier Oscar; Wang, Xisheng; Yi, Na; Barnes, Peter F.; García, Verónica Edith; Samten, Buka
Año de publicación
2018
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Cyclic adenosine monophosphate (cAMP) is critical in immune regulation, and its role in tuberculosis infection remains unclear. We determined the levels of cAMP in peripheral blood mononuclear cells (PBMC) from tuberculosis patients and the mechanisms for cAMP suppression of IFN-γ production. PBMC from tuberculosis patients contained significantly elevated cAMP than latent tuberculosis infected subjects (LTBI), with an inverse correlation with IFN-γ production. Consistent with this, the expression of cAMP response element binding protein (CREB), activating transcription factor (ATF)-2 and c-Jun were reduced in tuberculosis patients compared with LTBI. PKA type I specific cAMP analogs inhibited Mtb-stimulated IFN-g production by PBMC through suppression of Mtb-induced IFN-γ promoter binding activities of CREB, ATF-2, and c-Jun and also miR155, the target miRNA of these transcription factors. Neutralizing both IL-10 and TGF-β1 or supplementation of IL-12 restored cAMP-suppressed IFN-g production. We conclude that increased cAMP inhibits IFN-g production through PKA type I pathway in tuberculosis infection.
Fil: Yoon-tae Chung. University of California at Los Angeles. School of Medicine; Estados Unidos
Fil: Pasquineli, V. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; Argentina
Fil: J. Jurado. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; Argentina
Fil: Xisheng Wang. University of California at Los Angeles. School of Medicine; Estados Unidos
Fil: Na Yi. University of California at Los Angeles. School of Medicine; Estados Unidos
Fil: Peter Barnes. University of California at Los Angeles. School of Medicine; Estados Unidos
Fil: García, Verónica Edith. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; Argentina
Fil: Buka Samten. University of California at Los Angeles. School of Medicine; Estados Unidos
Materia
CYCLIC ADENOSINE MONOPHOSPHATE
CYTOKINE
HUMAN
TRANSCRIPTION FACTOR
TUBERCULOSIS
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:11336/93891
Acceder
id CONICETDig_16e832f20cca06576fcfd3b1fb6bc4f7
oai_identifier_str oai:ri.conicet.gov.ar:11336/93891
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Elevated cyclic AMP inhibits mycobacterium tuberculosis-stimulated T-cell IFN-γ secretion through type I protein kinase AChung, Yoon-taePasquinelli, VirginiaJurado, Javier OscarWang, XishengYi, NaBarnes, Peter F.García, Verónica EdithSamten, BukaCYCLIC ADENOSINE MONOPHOSPHATECYTOKINEHUMANTRANSCRIPTION FACTORTUBERCULOSIShttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Cyclic adenosine monophosphate (cAMP) is critical in immune regulation, and its role in tuberculosis infection remains unclear. We determined the levels of cAMP in peripheral blood mononuclear cells (PBMC) from tuberculosis patients and the mechanisms for cAMP suppression of IFN-γ production. PBMC from tuberculosis patients contained significantly elevated cAMP than latent tuberculosis infected subjects (LTBI), with an inverse correlation with IFN-γ production. Consistent with this, the expression of cAMP response element binding protein (CREB), activating transcription factor (ATF)-2 and c-Jun were reduced in tuberculosis patients compared with LTBI. PKA type I specific cAMP analogs inhibited Mtb-stimulated IFN-g production by PBMC through suppression of Mtb-induced IFN-γ promoter binding activities of CREB, ATF-2, and c-Jun and also miR155, the target miRNA of these transcription factors. Neutralizing both IL-10 and TGF-β1 or supplementation of IL-12 restored cAMP-suppressed IFN-g production. We conclude that increased cAMP inhibits IFN-g production through PKA type I pathway in tuberculosis infection.Fil: Yoon-tae Chung. University of California at Los Angeles. School of Medicine; Estados UnidosFil: Pasquineli, V. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; ArgentinaFil: J. Jurado. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; ArgentinaFil: Xisheng Wang. University of California at Los Angeles. School of Medicine; Estados UnidosFil: Na Yi. University of California at Los Angeles. School of Medicine; Estados UnidosFil: Peter Barnes. University of California at Los Angeles. School of Medicine; Estados UnidosFil: García, Verónica Edith. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; ArgentinaFil: Buka Samten. University of California at Los Angeles. School of Medicine; Estados UnidosUniversity of Chicago Press2018-06info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/93891Chung, Yoon-tae; Pasquinelli, Virginia; Jurado, Javier Oscar; Wang, Xisheng; Yi, Na; et al.; Elevated cyclic AMP inhibits mycobacterium tuberculosis-stimulated T-cell IFN-γ secretion through type I protein kinase A; University of Chicago Press; Journal Of Infectious Diseases; 217; 11; 6-2018; 1821-18310022-1899CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1093/infdis/jiy079info:eu-repo/semantics/altIdentifier/url/https://academic.oup.com/jid/article/217/11/1821/4845549info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:52:54Zoai:ri.conicet.gov.ar:11336/93891instacron: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:34982025-09-03 09:52:56.418CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Elevated cyclic AMP inhibits mycobacterium tuberculosis-stimulated T-cell IFN-γ secretion through type I protein kinase A
title Elevated cyclic AMP inhibits mycobacterium tuberculosis-stimulated T-cell IFN-γ secretion through type I protein kinase A
spellingShingle Elevated cyclic AMP inhibits mycobacterium tuberculosis-stimulated T-cell IFN-γ secretion through type I protein kinase A
Chung, Yoon-tae
CYCLIC ADENOSINE MONOPHOSPHATE
CYTOKINE
HUMAN
TRANSCRIPTION FACTOR
TUBERCULOSIS
title_short Elevated cyclic AMP inhibits mycobacterium tuberculosis-stimulated T-cell IFN-γ secretion through type I protein kinase A
title_full Elevated cyclic AMP inhibits mycobacterium tuberculosis-stimulated T-cell IFN-γ secretion through type I protein kinase A
title_fullStr Elevated cyclic AMP inhibits mycobacterium tuberculosis-stimulated T-cell IFN-γ secretion through type I protein kinase A
title_full_unstemmed Elevated cyclic AMP inhibits mycobacterium tuberculosis-stimulated T-cell IFN-γ secretion through type I protein kinase A
title_sort Elevated cyclic AMP inhibits mycobacterium tuberculosis-stimulated T-cell IFN-γ secretion through type I protein kinase A
dc.creator.none.fl_str_mv Chung, Yoon-tae
Pasquinelli, Virginia
Jurado, Javier Oscar
Wang, Xisheng
Yi, Na
Barnes, Peter F.
García, Verónica Edith
Samten, Buka
author Chung, Yoon-tae
author_facet Chung, Yoon-tae
Pasquinelli, Virginia
Jurado, Javier Oscar
Wang, Xisheng
Yi, Na
Barnes, Peter F.
García, Verónica Edith
Samten, Buka
author_role author
author2 Pasquinelli, Virginia
Jurado, Javier Oscar
Wang, Xisheng
Yi, Na
Barnes, Peter F.
García, Verónica Edith
Samten, Buka
author2_role author
author
author
author
author
author
author
dc.subject.none.fl_str_mv CYCLIC ADENOSINE MONOPHOSPHATE
CYTOKINE
HUMAN
TRANSCRIPTION FACTOR
TUBERCULOSIS
topic CYCLIC ADENOSINE MONOPHOSPHATE
CYTOKINE
HUMAN
TRANSCRIPTION FACTOR
TUBERCULOSIS
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Cyclic adenosine monophosphate (cAMP) is critical in immune regulation, and its role in tuberculosis infection remains unclear. We determined the levels of cAMP in peripheral blood mononuclear cells (PBMC) from tuberculosis patients and the mechanisms for cAMP suppression of IFN-γ production. PBMC from tuberculosis patients contained significantly elevated cAMP than latent tuberculosis infected subjects (LTBI), with an inverse correlation with IFN-γ production. Consistent with this, the expression of cAMP response element binding protein (CREB), activating transcription factor (ATF)-2 and c-Jun were reduced in tuberculosis patients compared with LTBI. PKA type I specific cAMP analogs inhibited Mtb-stimulated IFN-g production by PBMC through suppression of Mtb-induced IFN-γ promoter binding activities of CREB, ATF-2, and c-Jun and also miR155, the target miRNA of these transcription factors. Neutralizing both IL-10 and TGF-β1 or supplementation of IL-12 restored cAMP-suppressed IFN-g production. We conclude that increased cAMP inhibits IFN-g production through PKA type I pathway in tuberculosis infection.
Fil: Yoon-tae Chung. University of California at Los Angeles. School of Medicine; Estados Unidos
Fil: Pasquineli, V. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; Argentina
Fil: J. Jurado. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; Argentina
Fil: Xisheng Wang. University of California at Los Angeles. School of Medicine; Estados Unidos
Fil: Na Yi. University of California at Los Angeles. School of Medicine; Estados Unidos
Fil: Peter Barnes. University of California at Los Angeles. School of Medicine; Estados Unidos
Fil: García, Verónica Edith. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; Argentina
Fil: Buka Samten. University of California at Los Angeles. School of Medicine; Estados Unidos
description Cyclic adenosine monophosphate (cAMP) is critical in immune regulation, and its role in tuberculosis infection remains unclear. We determined the levels of cAMP in peripheral blood mononuclear cells (PBMC) from tuberculosis patients and the mechanisms for cAMP suppression of IFN-γ production. PBMC from tuberculosis patients contained significantly elevated cAMP than latent tuberculosis infected subjects (LTBI), with an inverse correlation with IFN-γ production. Consistent with this, the expression of cAMP response element binding protein (CREB), activating transcription factor (ATF)-2 and c-Jun were reduced in tuberculosis patients compared with LTBI. PKA type I specific cAMP analogs inhibited Mtb-stimulated IFN-g production by PBMC through suppression of Mtb-induced IFN-γ promoter binding activities of CREB, ATF-2, and c-Jun and also miR155, the target miRNA of these transcription factors. Neutralizing both IL-10 and TGF-β1 or supplementation of IL-12 restored cAMP-suppressed IFN-g production. We conclude that increased cAMP inhibits IFN-g production through PKA type I pathway in tuberculosis infection.
publishDate 2018
dc.date.none.fl_str_mv 2018-06
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/93891
Chung, Yoon-tae; Pasquinelli, Virginia; Jurado, Javier Oscar; Wang, Xisheng; Yi, Na; et al.; Elevated cyclic AMP inhibits mycobacterium tuberculosis-stimulated T-cell IFN-γ secretion through type I protein kinase A; University of Chicago Press; Journal Of Infectious Diseases; 217; 11; 6-2018; 1821-1831
0022-1899
CONICET Digital
CONICET
url http://hdl.handle.net/11336/93891
identifier_str_mv Chung, Yoon-tae; Pasquinelli, Virginia; Jurado, Javier Oscar; Wang, Xisheng; Yi, Na; et al.; Elevated cyclic AMP inhibits mycobacterium tuberculosis-stimulated T-cell IFN-γ secretion through type I protein kinase A; University of Chicago Press; Journal Of Infectious Diseases; 217; 11; 6-2018; 1821-1831
0022-1899
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1093/infdis/jiy079
info:eu-repo/semantics/altIdentifier/url/https://academic.oup.com/jid/article/217/11/1821/4845549
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv University of Chicago Press
publisher.none.fl_str_mv University of Chicago Press
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
_version_ 1842269189905055744
score 13.13397

Publicaciones similares