Evidence map›Paper›PMID 20197549›Full record

ArticleBlood2010

MyD88-dependent TLR4 signaling is selectively impaired in alveolar macrophages from asymptomatic HIV+ persons.

Souvenir D Tachado, Xin Li, Medhavi Bole, Katharine Swan, Asha Anandaiah, Naimish R Patel, Henry Koziel

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

21 citing papers in PubMed, 38 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Review
  6. Infection and atherosclerosis: TLR-dependent pathways.Cellular and molecular life sciences : CMLS · 2020
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Pathogenesis of HIV and the lung.Current HIV/AIDS reports · 2013
    Review
  17. Article
  18. Article
  19. Article
  20. Review
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

7 authors at 2 institutions in 1 country.

Souvenir D TachadoDivision of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA. stachado@bidmc.harvard.edu
Xin Li
Medhavi Bole
Katharine Swan
Asha Anandaiah
Naimish R Patel
Henry Koziel
Beth Israel Deaconess Medical Center · USHarvard University · US

Funding

ALVEOLAR MACROPHAGE INNATE IMMUNE FUNCTION IN HIVR01HL063655 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KOZIEL, HENRY · 2000 to 2010
$4.1M
HIV Compromises Lung Macrophage TLR Host Defense FunctionR01HL092811 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TACHADO, SOUVENIR D · 2009 to 2013
$2.1M
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 HL063655NHLBI NIH HHS R01-HL063655NHLBI NIH HHS R01 HL092811NHLBI NIH HHS R01-HL092811NIAID NIH HHS K08 AI064014NIAID NIH HHS K08-AI064014
6 · The paper itself

Abstract

Alveolar macrophages (AMs) are the predominant effector cell in the lungs and contribute to a critical first line of defense against bacterial pathogens through recognition by pattern recognition receptors such as Toll-like receptor 4 (TLR4). TLR4-mediated tumor necrosis factor alpha (TNFalpha) release is significantly impaired in HIV(+) macrophages, but whether HIV impairs myeloid differentiation factor 88 (MyD88)-dependent and/or MyD-independent TLR4 signaling pathways in human macrophages is not known. Comparing human U937 macrophages with HIV(+) U1 macrophages (HIV-infected U937 subclone), the current study shows that HIV infection is associated with impaired macrophage TLR4-mediated signaling, specifically targeting the MyD88-dependent TLR4-mediated signaling pathway (reduced MyD88-interleukin-1 receptor-associated kinase [IRAK] interaction, IRAK phosphorylation, nuclear factor [NF]-kappaB nuclear translocation, and TNFalpha release) while preserving the MyD88-independent TLR4-mediated signaling pathway (preserved STAT1 phosphorylation, interferon regulatory factor [IRF] nuclear translocation, and interleukin-10 [IL-10] and RANTES release). Extracellular TLR4 signaling complex was intact (similar levels of CD14 and MD2), and similar patterns of response were observed in clinically relevant AMs from healthy and asymptomatic HIV(+) persons at high clinical risk of pneumonia. Taken together, these data support the concept that chronic HIV infection is associated with specific and targeted disruption of critical macrophage TLR4 signaling, which in turn may contribute to disease pathogenesis of bacterial pneumonia.

Indexed as

HIVSignal TransductionActive Transport, Cell NucleusCell NucleusCytokinesFemaleHIV InfectionsHumansInterferon Regulatory FactorsInterleukin-1 Receptor-Associated KinasesMacrophages, AlveolarMaleMyeloid Differentiation Factor 88PhosphorylationPneumoniaRiskCytokinesInterferon Regulatory FactorsInterleukin-1 Receptor-Associated KinasesMYD88 protein, humanMyeloid Differentiation Factor 88TLR4 protein, humanToll-Like Receptor 4

Identifiers

PMID20197549
PMCPMC2867269
OpenAlexW2006960117

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.