Evidence map›Paper›PMID 19383626›Full record

ArticleJournal of leukocyte biology2009

Impaired M. tuberculosis-mediated apoptosis in alveolar macrophages from HIV+ persons: potential role of IL-10 and BCL-3.

Naimish R Patel, Katharine Swan, Xin Li, Souvenir D Tachado, Henry Koziel

Abstract read
In one paragraph

Article in Journal of leukocyte biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

37 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
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  15. Striking the right immunological balance prevents progression of tuberculosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017
    Review
  16. Pulmonary Innate Immune Dysfunction in Human Immunodeficiency Virus.American journal of respiratory cell and molecular biology · 2017
    Review
  17. Review
  18. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Naimish R PatelDivision of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA. npatel@bidmc.harvard.edu
Katharine Swan
Xin Li
Souvenir D Tachado
Henry Koziel
Beth Israel Deaconess Medical Center · US

Funding

ALVEOLAR MACROPHAGE INNATE IMMUNE FUNCTION IN HIVR01HL063655 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KOZIEL, HENRY · 2000 to 2010
$4.1M
Lung macrophage innate receptor response to MTb in HIVK08AI064014 · NIAID · BETH ISRAEL DEACONESS MEDICAL CENTER · PI PATEL, NAIMISH RAMESH · 2005 to 2009
$596k
NHLBI NIH HHS R01-HL063655NIAID NIH HHS K08-AI064014
6 · The paper itself

Abstract

The mechanism of increased MTb disease susceptibility in HIV+ persons remains poorly understood. Apoptosis of macrophages in response to MTb represents a critical host defense response, and decreased apoptosis may represent a mechanism of increased susceptibility to MTb in HIV. In the current study, MTb-mediated apoptosis of human AM was reduced in HIV+ subjects compared with healthy subjects in a TNF-alpha-dependent manner. IL-10 levels in BALF from HIV+ persons were significantly elevated compared with HIV- persons, and exogenous IL-10 reduced MTb-mediated apoptosis in healthy AM, suggesting that IL-10 could mediate decreased apoptosis observed in HIV. Further study showed that IL-10 reduced TNF release in response to MTb in AM through a reduction in TNF mRNA levels, and exogenous TNF could partially reverse IL-10-associated effects on AM apoptosis. IL-10 did not influence p-IRAK, IkappaB degradation, or NF-kappaB p65 nuclear translocation in response to MTb, but IL-10 did increase levels of AM BCL-3, an inhibitor of NF-kappaB nuclear activity. BCL-3 knockdown in human macrophages increased MTb-mediated TNF release. Importantly, BCL-3 levels in AM from HIV+ subjects were higher compared with healthy subjects. Taken together, these data suggest that elevated lung levels of IL-10 may impair MTb-mediated AM apoptosis in HIV through a BCL-3-dependent mechanism. BCL-3 may represent a potential therapeutic target to treat or prevent MTb disease in HIV+ persons.

Indexed as

ApoptosisB-Cell Lymphoma 3 ProteinDisease SusceptibilityHIV InfectionsHumansImmunity, InnateInterleukin-10LungMacrophages, AlveolarNF-kappa BProto-Oncogene ProteinsTranscription FactorsTuberculosisB-Cell Lymphoma 3 ProteinBCL3 protein, humanInterleukin-10NF-kappa BProto-Oncogene ProteinsTranscription Factors

Identifiers

PMID19383626
PMCPMC2704623
OpenAlexW2128827386

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.