Evidence map›Paper›PMID 31226436›Full record

Trial reportCytokine2019

Changes in inflammatory protein and lipid mediator profiles persist after antitubercular treatment of pulmonary and extrapulmonary tuberculosis: A prospective cohort study.

Caian L Vinhaes, Deivide Oliveira-de-Souza, Paulo S Silveira-Mattos, Betania Nogueira, Ruiru Shi, Wang Wei, Xing Yuan, Guolong Zhang, Ying Cai, Clifton E Barry and 4 more

Open access · greenAbstract readClinical TrialMulticenter Study
In one paragraph

Trial report in Cytokine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
5.2field-weighted citation impact, top 3% 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

36 citing papers in PubMed, 54 citations in OpenAlex.

  1. Trial
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  3. Compartment-specific inflammation in tuberculous lymphadenitis: a case-control study.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  11. MedComm · 2023
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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

14 authors at 6 institutions in 4 countries.

Caian L VinhaesInstituto Gonçalo Moniz, Fundação Oswaldo Cruz, Salvador 40296-710, Brazil; Multinational Organization Network Sponsoring Translational and Epidemiological Research (MONSTER) Initiative, Fundação José Silveira, Salvador 40210-320, Brazil; Curso de Medicina, Faculdade de Tecnologia e Ciências (FTC), Salvador 40290-150, Brazil.
Deivide Oliveira-de-SouzaInstituto Gonçalo Moniz, Fundação Oswaldo Cruz, Salvador 40296-710, Brazil; Multinational Organization Network Sponsoring Translational and Epidemiological Research (MONSTER) Initiative, Fundação José Silveira, Salvador 40210-320, Brazil; Curso de Medicina, Faculdade de Tecnologia e Ciências (FTC), Salvador 40290-150, Brazil.
Paulo S Silveira-MattosInstituto Gonçalo Moniz, Fundação Oswaldo Cruz, Salvador 40296-710, Brazil; Multinational Organization Network Sponsoring Translational and Epidemiological Research (MONSTER) Initiative, Fundação José Silveira, Salvador 40210-320, Brazil; Curso de Medicina, Faculdade de Tecnologia e Ciências (FTC), Salvador 40290-150, Brazil.
Betania NogueiraMultinational Organization Network Sponsoring Translational and Epidemiological Research (MONSTER) Initiative, Fundação José Silveira, Salvador 40210-320, Brazil.
Ruiru ShiHenan Chest Hospital, Zhengzhou 450000, China.
Wang WeiHenan Chest Hospital, Zhengzhou 450000, China.
Xing YuanHenan Chest Hospital, Zhengzhou 450000, China.
Guolong ZhangHenan Anti-TB Institute, Sino-US Joint Research Laboratory for Tuberculosis of Henan CDC, Zhengzhou 450000, China.
Ying CaiTuberculosis Research Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda 20892, MD, USA.
Clifton E BarryTuberculosis Research Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda 20892, MD, USA.
Laura E ViaTuberculosis Research Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda 20892, MD, USA.
Kiyoshi F FukutaniInstituto Gonçalo Moniz, Fundação Oswaldo Cruz, Salvador 40296-710, Brazil; Multinational Organization Network Sponsoring Translational and Epidemiological Research (MONSTER) Initiative, Fundação José Silveira, Salvador 40210-320, Brazil; Curso de Medicina, Faculdade de Tecnologia e Ciências (FTC), Salvador 40290-150, Brazil.
Bruno B AndradeInstituto Gonçalo Moniz, Fundação Oswaldo Cruz, Salvador 40296-710, Brazil; Multinational Organization Network Sponsoring Translational and Epidemiological Research (MONSTER) Initiative, Fundação José Silveira, Salvador 40210-320, Brazil; Curso de Medicina, Faculdade de Tecnologia e Ciências (FTC), Salvador 40290-150, Brazil; Escola Bahiana de Medicina e Saúde Pública (EBMSP), Salvador 40290-000, Brazil; Universidade Salvador (UNIFACS), Laureate Universities, Salvador 41720-200, Brazil; Wellcome Centre for Infectious Disease Research in Africa, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Cape Town 7925, South Africa; Division of Infectious Diseases, Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232, USA. Electronic address: bruno.andrade@fiocruz.br.
Katrin D Mayer-BarberInflammation and Innate Immunity Unit, Laboratory of Clinical Immunology and Microbiology, NIAID, NIH, Bethesda 20892, MD, USA. Electronic address: mayerk@niaid.nih.gov.
Faculdade de Tecnologia e Ciências · BRHenan Provincial Chest Hospital · CNNational Institutes of Health · USEscola Bahiana de Medicina e Saúde Pública · BRHenan Provincial Center for Disease Control and Prevention · CNNational Institute of Allergy and Infectious Diseases · US

Funding

CCASAnet: Caribbean, Central and South America NetworkU01AI069923 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Pedro Enrique Cahn, Jessica L Castilho · 2006 to 2026
$41.6M
Innate inflammatory responses during pulmonary infectionsZIAAI001207 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MAYER-BARBER, KATRIN · 2015 to 2025
$13.6M
International Tuberculosis Research in ChinaZIAAI001081 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI BARRY, CLIFTON · 2010 to 2025
$12.2M
Inflammatory determinants of disease severity and treatment outcome in TB patientsU01AI115940 · NIAID · UNIVERSITY OF CAPE TOWN · PI SHER, ALAN, WILKINSON, ROBERT JOHN · 2015 to 2019
$1.1M
Intramural NIH HHS ZIA AI001207NIAID NIH HHS U01 AI069923NIAID NIH HHS U01 AI115940
6 · The paper itself

Abstract

backgroundThe identification of meaningful biomarkers of tuberculosis (TB) has potential to improve diagnosis, disease staging and prediction of treatment outcomes. It has been shown that active pulmonary TB (PTB) is associated with qualitative and quantitative changes in systemic immune profile, suggesting a chronic inflammatory imbalance. Here we characterized the profile of PTB and extrapulmonary TB (EPTB) in a prospective cohort study.

methodsWe measured a panel of 27 inflammatory cytokines, soluble receptors, and lipid mediators in peripheral blood from patients with PTB or EPTB from a prospective clinical study in China. Multidimensional analyses were performed to describe associations between plasma levels of biomarkers and different TB disease presentation profiles.

resultsMycobacterium tuberculosis infection induced changes in both the expression and correlation profiles of plasma mediators of inflammation in patients with PTB compared to those with EPTB. Increases in mycobacterial loads in sputum smears were associated with rises in concentrations of several molecules involved in TB pathogenesis, such as IL-1β, IFN-α, IL-10 and PGF2α. Moreover, PTB patients presenting with severe disease exhibited a distinct inflammatory profile hallmarked by heightened levels of TNF-α, IL-1β, IL17, IL-18 and IL-27. Interestingly, while antitubercular treatment (ATT) resulted in early changes of plasma concentrations of markers in PTB, changes were delayed in EPTB patients. Exploratory analyses of the molecular degree of perturbation (MDP) of the inflammatory mediators before and during ATT suggested the occurrence of infection and/or treatment-induced long lasting "inflammatory imprinting" of biomarker profiles in TB. At 24 weeks post ATT commencement, markers underlying the observed increases in MDP scores were IL-27 in PTB and IL-1β in EPTB patients.

conclusionOur findings describe systemic and durable changes in the concentrations of inflammatory cytokines and lipid mediators in both PTB and EPTB and emphasize the role of M. tuberculosis bacterial burden and site of disease in modulating patient immune biomarkers.

Indexed as

CytokinesLipidsMycobacterium tuberculosisTuberculosis, PulmonaryAdultAntitubercular AgentsBiomarkersFemaleHumansMaleMiddle AgedProspective StudiesAntitubercular AgentsBiomarkersCytokinesLipidsAcid-fast bacilliCytokinesExtrapulmonary tuberculosisInflammationLipid mediatorMycobacterium tuberculosis

Identifiers

PMID31226436
PMCPMC6739167
OpenAlexW2953124793

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Registered trials

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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.