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

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 f...

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Autor principal: Chung, Y.-T
Otros Autores: Pasquinelli, V., Jurado, J.O, Wang, X., Yi, N., Barnes, P.F, Garcia, V.E, Samten, B.
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: Oxford University Press 2018
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Acceso en línea:Registro en Scopus
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024 7 |2 cas  |a cyclic AMP, 60-92-4; cyclic AMP responsive element binding protein, 130428-87-4, 130939-96-7; gamma interferon, 82115-62-6; interleukin 12, 138415-13-1 
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030 |a JIDIA 
100 1 |a Chung, Y.-T. 
245 1 0 |a Elevated cyclic AMP inhibits mycobacterium tuberculosis-stimulated T-cell IFN-γ secretion through type I protein kinase A 
260 |b Oxford University Press  |c 2018 
270 1 0 |m Samten, B.; Department of Pulmonary Immunology, University of Texas Health Science Center, 11937 US Hwy 271, United States; email: buka.samten@uthct.edu 
506 |2 openaire  |e Política editorial 
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520 3 |a 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. © The Author(s) 2018. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved.  |l eng 
536 |a Detalles de la financiación: Texas A and M University Health Science Center 
536 |a Detalles de la financiación: Universidad Nacional del Centro de la Provincia de Buenos Aires 
536 |a Detalles de la financiación: Universidad de Buenos Aires 
536 |a Detalles de la financiación: Facultad de Ciencias Físicas y Matemáticas 
536 |a Detalles de la financiación: Consejo Nacional de Investigaciones Científicas y Técnicas 
536 |a Detalles de la financiación: Consejo Nacional de Investigaciones Científicas y Técnicas 
536 |a Detalles de la financiación: Texas A and M University Health Science Center 
536 |a Detalles de la financiación: National Institutes of Health, 1R56AI116864 
536 |a Detalles de la financiación: 1Department of Pulmonary Immunology, University of Texas Health Science Center, Tyler; 2Centro de Investigaciones y Transferencia del Noroeste de la Provincia de Buenos Aires, Universidad Nacional del Noroeste de la Provincia de Buenos Aires-Consejo Nacional de Investigaciones Científicas y Técnicas, Junín, Argentina; and 3Departamento de Química Biológica, and Consejo Nacional de Investigaciones Científicas y Técnicas, Instituto de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Argentina 
536 |a Detalles de la financiación: Financial support. This work was supported in part by the funds from the National Institutes of Health (grant number 1R56AI116864) and the University of Texas Health Science Center at Tyler, Texas. 
593 |a Centro de Investigaciones y Transferencia del Noroeste de la Provincia de Buenos Aires, Universidad Nacional del Noroeste de la Provincia de Buenos Aires- Consejo Nacional de Investigaciones Científicas y Técnicas, Junín, Argentina 
593 |a Departamento de Química Biológica, Consejo Nacional de Investigaciones Científicas y Técnicas, Instituto de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Argentina 
593 |a Department of Vet Biomedical Sciences, Oregon State University, United States 
593 |a Department of Pulmonary Immunology, University of Texas Health Science Center, 11937 US Hwy 271, Tyler, TX 75708-3154, United States 
690 1 0 |a CYCLIC ADENOSINE MONOPHOSPHATE 
690 1 0 |a CYTOKINE 
690 1 0 |a HUMAN 
690 1 0 |a TRANSCRIPTION FACTOR 
690 1 0 |a ACTIVATING TRANSCRIPTION FACTOR 2 
690 1 0 |a CYCLIC AMP 
690 1 0 |a CYCLIC AMP DEPENDENT PROTEIN KINASE 1 
690 1 0 |a CYCLIC AMP RESPONSIVE ELEMENT BINDING PROTEIN 
690 1 0 |a GAMMA INTERFERON 
690 1 0 |a INTERLEUKIN 10 
690 1 0 |a INTERLEUKIN 12 
690 1 0 |a MICRORNA 155 
690 1 0 |a PROTEIN C JUN 
690 1 0 |a TRANSFORMING GROWTH FACTOR BETA1 
690 1 0 |a ARTICLE 
690 1 0 |a CONTROLLED STUDY 
690 1 0 |a CYTOKINE PRODUCTION 
690 1 0 |a CYTOKINE RELEASE 
690 1 0 |a GEL MOBILITY SHIFT ASSAY 
690 1 0 |a GENE EXPRESSION 
690 1 0 |a HUMAN 
690 1 0 |a HUMAN CELL 
690 1 0 |a LATENT TUBERCULOSIS 
690 1 0 |a LUNG TUBERCULOSIS 
690 1 0 |a MAJOR CLINICAL STUDY 
690 1 0 |a MYCOBACTERIUM TUBERCULOSIS 
690 1 0 |a NONHUMAN 
690 1 0 |a PERIPHERAL BLOOD MONONUCLEAR CELL 
690 1 0 |a PRIORITY JOURNAL 
690 1 0 |a PROTEIN EXPRESSION 
690 1 0 |a WESTERN BLOTTING 
650 1 7 |2 spines  |a TUBERCULOSIS 
700 1 |a Pasquinelli, V. 
700 1 |a Jurado, J.O. 
700 1 |a Wang, X. 
700 1 |a Yi, N. 
700 1 |a Barnes, P.F. 
700 1 |a Garcia, V.E. 
700 1 |a Samten, B. 
773 0 |d Oxford University Press, 2018  |g v. 217  |h pp. 1821-1831  |k n. 11  |p J. Infect. Dis.  |x 00221899  |w (AR-BaUEN)CENRE-5621  |t Journal of Infectious Diseases 
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