Evidence map›Paper›PMID 28414762›Full record

ArticlePloS one2017

Transcriptional networks are associated with resistance to Mycobacterium tuberculosis infection.

Chetan Seshadri, Nafiseh Sedaghat, Monica Campo, Glenna Peterson, Richard D Wells, Gregory S Olson, David R Sherman, Catherine M Stein, Harriet Mayanja-Kizza, Ali Shojaie and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

46 citing papers in PubMed, 68 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
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  5. Experimental dissection of tuberculosis protective immunity: a human perspective.Frontiers in cellular and infection microbiology · 2025
    Review
  6. Article
  7. Specific CD4Nature immunology · 2024
    Article
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  13. microLife · 2023
    Article
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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

13 authors at 5 institutions in 3 countries.

Chetan SeshadriDepartment of Medicine, University of Washington, Seattle, Washington, United States of America.ORCID http://orcid.org/0000-0003-2783-7540
Nafiseh SedaghatComputer Engineering School, Iran University of Science and Technology, Tehran, Iran.
Monica CampoDepartment of Medicine, University of Washington, Seattle, Washington, United States of America.
Glenna PetersonDepartment of Medicine, University of Washington, Seattle, Washington, United States of America.
Richard D WellsDepartment of Medicine, University of Washington, Seattle, Washington, United States of America.
Gregory S OlsonDepartment of Medicine, University of Washington, Seattle, Washington, United States of America.
David R ShermanCenter for Infectious Disease Research, Seattle, Washington.
Catherine M SteinDepartment of Epidemiology & Biostatistics, Case Western Reserve University, Cleveland, Ohio, United States of America.
Harriet Mayanja-KizzaMakerere University, Kampala, Uganda.
Ali ShojaieDepartment of Biostatistics, University of Washington, Seattle, Washington, United States of America.
W Henry BoomDepartment of Medicine, Case Western Reserve University, Cleveland, Ohio, United States of America.
Thomas R HawnDepartment of Medicine, University of Washington, Seattle, Washington, United States of America.
Tuberculosis Research Unit (TBRU)
University of Washington · USCase Western Reserve University · USCenter for Infectious Disease Research · USIran University of Science and Technology · IRMakerere University · UG

Funding

University of Washington Medical Scientist Training Program: MD/PhDT32GM007266 · NIGMS · UNIVERSITY OF WASHINGTON · PI HORWITZ, MARSHALL S. · 1985 to 2023
$30.4M
NCCIH Supplement to NCATS/CTSA Program for KL2 Scholars - M. SoddersKL2TR002317 · NCATS · UNIVERSITY OF WASHINGTON · PI Christy Michelle McKinney · 2017 to 2026
$14.5M
Resistance to MTB infection in HIV infected individuals in Uganda and S. AfricaR01AI124348 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI BOOM, W. HENRY, HAWN, THOMAS R · 2016 to 2020
$11.3M
Tuberculosis Prevention Research Unit /TBRU/-266095383N01AI095383 · NIAID · CASE WESTERN RESERVE UNIVERSITY · 2000 to 2005
$5.6M
Natural Resistance to Mycobacterium Tuberculosis InfectionU01AI115642 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI BOOM, W. HENRY, MAYANJA-KIZZA, HARRIET · 2015 to 2019
$3.5M
Machine Learning Tools for Discovery and Analysis of Active Metabolic PathwaysR01GM114029 · NIGMS · UNIVERSITY OF WASHINGTON · PI SHOJAIE, ALI · 2016 to 2020
$1.7M
Statistical Methods for Network-Based Integrative Analysis of CVD Epigenetic DataK01HL124050 · NHLBI · UNIVERSITY OF WASHINGTON · PI SHOJAIE, ALI · 2016 to 2020
$693k
NCATS NIH HHS KL2 TR002317NHLBI NIH HHS K01 HL124050NIAID NIH HHS N01 AI070022NIAID NIH HHS N01 AI095383NIAID NIH HHS R01 AI124348NIAID NIH HHS U01 AI115642NIGMS NIH HHS R01 GM114029NIGMS NIH HHS T32 GM007266
6 · The paper itself

Abstract

rationaleUnderstanding mechanisms of resistance to M. tuberculosis (M.tb) infection in humans could identify novel therapeutic strategies as it has for other infectious diseases, such as HIV.

objectivesTo compare the early transcriptional response of M.tb-infected monocytes between Ugandan household contacts of tuberculosis patients who demonstrate clinical resistance to M.tb infection (cases) and matched controls with latent tuberculosis infection.

methodsCases (n = 10) and controls (n = 18) were selected from a long-term household contact study in which cases did not convert their tuberculin skin test (TST) or develop tuberculosis over two years of follow up. We obtained genome-wide transcriptional profiles of M.tb-infected peripheral blood monocytes and used Gene Set Enrichment Analysis and interaction networks to identify cellular processes associated with resistance to clinical M.tb infection. MEASUREMENTS AND MAIN

resultsWe discovered gene sets associated with histone deacetylases that were differentially expressed when comparing resistant and susceptible subjects. We used small molecule inhibitors to demonstrate that histone deacetylase function is important for the pro-inflammatory response to in-vitro M.tb infection in human monocytes.

conclusionsMonocytes from individuals who appear to resist clinical M.tb infection differentially activate pathways controlled by histone deacetylase in response to in-vitro M.tb infection when compared to those who are susceptible and develop latent tuberculosis. These data identify a potential cellular mechanism underlying the clinical phenomenon of resistance to M.tb infection despite known exposure to an infectious contact.

Indexed as

AdolescentAdultCase-Control StudiesCytokinesDrug Resistance, BacterialFemaleGene Regulatory NetworksHumansInflammationLatent TuberculosisMaleMonocytesMycobacterium tuberculosisSmall Molecule LibrariesTranscription, GeneticTuberculosis, PulmonaryCytokinesSmall Molecule Libraries

Identifiers

PMID28414762
PMCPMC5393882
OpenAlexW2605882561

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.