Evidence map›Paper›PMID 27793104›Full record

ArticleBMC microbiology2016

N-acetyl-cysteine exhibits potent anti-mycobacterial activity in addition to its known anti-oxidative functions.

Eduardo P Amaral, Elisabete L Conceição, Diego L Costa, Michael S Rocha, Jamocyr M Marinho, Marcelo Cordeiro-Santos, Maria Regina D'Império-Lima, Theolis Barbosa, Alan Sher, Bruno B Andrade

Open access · goldAbstract read
In one paragraph

Article in BMC microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

72 citing papers in PubMed, 118 citations in OpenAlex.

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  9. Additive Effects ofInternational journal of molecular sciences · 2025
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  17. Diseases (Basel, Switzerland) · 2024
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12 more citing papers are in PubMed but not listed here.

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

10 authors at 6 institutions in 2 countries.

Eduardo P AmaralImmunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.
Elisabete L ConceiçãoLaboratório Integrado de Microbiologia e Imunorregulação (LIMI), Instituto Gonçalo Moniz, Fundação Oswaldo Cruz (FIOCRUZ), Salvador, 40296-710, Bahia, Brazil.
Diego L CostaImmunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.
Michael S RochaLaboratório Integrado de Microbiologia e Imunorregulação (LIMI), Instituto Gonçalo Moniz, Fundação Oswaldo Cruz (FIOCRUZ), Salvador, 40296-710, Bahia, Brazil.
Jamocyr M MarinhoDepartament of Internal Medicine, School of Medicine and Public Health, Salvador, 41150-100, Brazil.
Marcelo Cordeiro-SantosDepartamento de Ensino e Pós-Graduação, Fundação de Medicina Tropical Dr. Heitor Vieira Dourado, Manaus, Brazil.
Maria Regina D'Império-LimaDepartment of Immunology, Laboratory of Immunology of Infectious Diseases, Institute of Biomedical Science, University of São Paulo, São Paulo, 05508-900, Brazil.
Theolis BarbosaLaboratório Integrado de Microbiologia e Imunorregulação (LIMI), Instituto Gonçalo Moniz, Fundação Oswaldo Cruz (FIOCRUZ), Salvador, 40296-710, Bahia, Brazil.
Alan SherImmunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.
Bruno B AndradeImmunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, 20892, USA. bruno.andrade@bahia.fiocruz.br.
Fundação Oswaldo Cruz · BRNational Institute of Allergy and Infectious Diseases · USHospital São Rafael · BRNational Institutes of Health · USUniversidade de São Paulo · BRUniversidade do Estado do Amazonas · BR

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
Regulation Of Immunopathology In Bacterial And Parasitic DiseaseZIAAI000843 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI SHER, ALAN · 2009 to 2022
$11.1M
NIAID NIH HHS U01 AI069923
6 · The paper itself

Abstract

backgroundMycobacterium tuberculosis infection is thought to induce oxidative stress. N-acetyl-cysteine (NAC) is widely used in patients with chronic pulmonary diseases including tuberculosis due to its mucolytic and anti-oxidant activities. Here, we tested whether NAC exerts a direct antibiotic activity against mycobacteria.

methodsOxidative stress status in plasma was compared between pulmonary TB (PTB) patients and those with latent M. tuberculosis infection (LTBI) or healthy uninfected individuals. Lipid peroxidation, DNA oxidation and cell death, as well as accumulation of reactive oxygen species (ROS) were measured in cultures of primary human monocyte-derived macrophages infected with M. tuberculosis and treated or not with NAC. M. tuberculosis, M. avium and M. bovis BCG cultures were also exposed to different doses of NAC with or without medium pH adjustment to control for acidity. The anti-mycobacterial effect of NAC was assessed in M. tuberculosis infected human THP-1 cells and bone marrow-derived macrophages from mice lacking a fully functional NADPH oxidase system. The capacity of NAC to control M. tuberculosis infection was further tested in vivo in a mouse (C57BL/6) model.

resultsPTB patients exhibited elevated levels of oxidation products and a reduction of anti-oxidants compared with LTBI cases or uninfected controls. NAC treatment in M. tuberculosis-infected human macrophages resulted in a decrease of oxidative stress and cell death evoked by mycobacteria. Importantly, we observed a dose-dependent reduction in metabolic activity and in vitro growth of NAC treated M. tuberculosis, M. avium and M. bovis BCG. Furthermore, anti-mycobacterial activity in infected macrophages was shown to be independent of the effects of NAC on the host NADPH oxidase system in vitro. Short-term NAC treatment of M. tuberculosis infected mice in vivo resulted in a significant reduction of mycobacterial loads in the lungs.

conclusionsNAC exhibits potent anti-mycobacterial effects and may limit M. tuberculosis infection and disease both through suppression of the host oxidative response and through direct antimicrobial activity.

Indexed as

AcetylcysteineAdolescentAdultAnimalsAnti-Bacterial AgentsAntioxidantsCase-Control StudiesCell DeathCell LineDisease Models, AnimalHumansLatent TuberculosisLipid PeroxidationMacrophagesMaleMiceAcetylcysteineAnti-Bacterial AgentsAntioxidantsNADPH OxidasesReactive Oxygen SpeciesAntimicrobial activityN-acetyl cysteineTherapyTuberculosis

Identifiers

PMID27793104
PMCPMC5084440
OpenAlexW2545393754

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.