Evidence map›Paper›PMID 22778761›Full record

ArticleClinical & developmental immunology2012

Clinical isolates of Mycobacterium tuberculosis differ in their ability to induce respiratory burst and apoptosis in neutrophils as a possible mechanism of immune escape.

María M Romero, Luciana Balboa, Juan I Basile, Beatriz López, Viviana Ritacco, Silvia S de la Barrera, María C Sasiain, Lucía Barrera, Mercedes Alemán

Open access · goldAbstract read
In one paragraph

Article in Clinical & developmental immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. The Immune Escape Mechanisms ofInternational journal of molecular sciences · 2019
    Review
  5. Review
  6. Transmissible Mycobacterium tuberculosis Strains Share Genetic Markers and Immune Phenotypes.American journal of respiratory and critical care medicine · 2017
    Article
  7. Review
  8. Mediators of inflammation · 2017
    Article
  9. Article
  10. Article
  11. Nontuberculous mycobacterial osteomyelitis.Infectious diseases (London, England) · 2015
    Review
  12. Article
  13. Cell death and autophagy in tuberculosis.Seminars in immunology · 2014
    Review
  14. Article
  15. Article
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

9 authors at 2 institutions in 1 country.

María M RomeroIMEX-CONICET-ANM, Academia Nacional de Medicina, 1425 Buenos Aires, Argentina.
Luciana Balboa
Juan I Basile
Beatriz López
Viviana Ritacco
Silvia S de la Barrera
María C Sasiain
Lucía Barrera
Mercedes Alemán
Consejo Nacional de Investigaciones Científicas y Técnicas · ARAcademia Nacional de Medicina · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tuberculosis pathogenesis was earlier thought to be mainly related to the host but now it appears to be clear that bacterial factors are also involved. Genetic variability of Mycobacterium tuberculosis (Mtb) could be slight but it may lead to sharp phenotypic differences. We have previously reported that nonopsonized Mtb H37Rv induce apoptosis of polymorphonuclear neutrophils (PMNs) by a mechanism that involves the p38 pathway. Here we evaluated the capability to induce PMN apoptosis of two prevalent Mtb lineages in Argentina, the Latin America and Mediterranean (LAM), and Haarlem, using the H37Rv as a reference strain. Results showed that LAM strains strongly induced apoptosis of PMN which correlated with the induction of reactive oxygen species (ROS) production and p38 activation. Interestingly, the highly prosperous multidrug-resistant M strain, belonging to the Haarlem lineage, lacked the ability to activate and to induce PMN apoptosis as a consequence of (1) a weak ROS production and (2) the contribution of antiapoptotic mechanisms mediated at least by ERK. Although with less skill, M is able to enter the PMN so that phenotypic differences could lead PMN to be a reservoir allowing some pathogens to prevail and persist over other strains in the community.

Indexed as

Antigens, CDApoptosisCD11b AntigenCell Adhesion MoleculesExtracellular Signal-Regulated MAP KinasesGPI-Linked ProteinsHumansMycobacterium tuberculosisNeutrophilsp38 Mitogen-Activated Protein KinasesPhagocytosisReactive Oxygen SpeciesRespiratory BurstUp-RegulationAntigens, CDCD11b AntigenCEACAM8 protein, humanCell Adhesion MoleculesExtracellular Signal-Regulated MAP KinasesGPI-Linked Proteinsp38 Mitogen-Activated Protein KinasesReactive Oxygen Species

Identifiers

PMID22778761
PMCPMC3388301
OpenAlexW2082122766

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.