Evidence map›Paper›PMID 29438524›Full record

ArticleThe Journal of infectious diseases2018

Elevated Cyclic AMP Inhibits Mycobacterium tuberculosis-Stimulated T-cell IFN-γ Secretion Through Type I Protein Kinase A.

Yoon-Tae Chung, Virginia Pasquinelli, Javier O Jurado, Xisheng Wang, Na Yi, Peter F Barnes, Veronica E Garcia, Buka Samten

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of infectious diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.0field-weighted citation impact, top 26% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Lactate Metabolism and Signaling in Tuberculosis and Cancer: A Comparative Review.Frontiers in cellular and infection microbiology · 2021
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Yoon-Tae ChungDepartment of Pulmonary Immunology, University of Texas Health Science Center, Tyler.
Virginia PasquinelliCentro 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.
Javier O JuradoDepartamento 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.
Xisheng WangDepartment of Pulmonary Immunology, University of Texas Health Science Center, Tyler.
Na YiDepartment of Pulmonary Immunology, University of Texas Health Science Center, Tyler.
Peter F BarnesDepartment of Pulmonary Immunology, University of Texas Health Science Center, Tyler.
Veronica E GarciaDepartamento 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.
Buka SamtenDepartment of Pulmonary Immunology, University of Texas Health Science Center, Tyler.
The University of Texas Health Science Center at Tyler · USUniversity of Buenos Aires · ARConsejo Nacional de Investigaciones Científicas y Técnicas · AR

Funding

Mycobacterium tuberculosis proliferation and its regulationR56AI116864 · NIAID · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI SAMTEN, BUKA · 2015 to 2015
$358k
NIAID NIH HHS R56 AI116864
6 · The paper itself

Abstract

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.

Indexed as

Activating Transcription Factor 2Antigens, BacterialCyclic AMPCyclic AMP-Dependent Protein Kinase Type IHumansInterferon-gammaInterleukin-10Latent TuberculosisLeukocytes, MononuclearMycobacterium tuberculosisPromoter Regions, GeneticProtein BindingSignal TransductionT-LymphocytesActivating Transcription Factor 2Antigens, BacterialCyclic AMPCyclic AMP-Dependent Protein Kinase Type IInterferon-gammaInterleukin-10

Identifiers

PMID29438524
PMCPMC5946837
OpenAlexW2791739928

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.