Evidence map›Paper›PMID 15155616›Full record

ArticleInfection and immunity2004

Pneumocystis activates human alveolar macrophage NF-kappaB signaling through mannose receptors.

Jianmin Zhang, Jinping Zhu, Amy Imrich, Melanie Cushion, T Bernard Kinane, Henry Koziel

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

45 citing papers in PubMed, 96 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Keratinocyte Response to Infection withJournal of fungi (Basel, Switzerland) · 2022
    Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Adaptive immunity to fungi.Cold Spring Harbor perspectives in medicine · 2014
    Review
  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

6 authors at 3 institutions in 1 country.

Jianmin ZhangDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA.
Jinping Zhu
Amy Imrich
Melanie Cushion
T Bernard Kinane
Henry Koziel
Harvard University · USMassachusetts General Hospital · USUniversity of Cincinnati · US

Funding

ALVEOLAR MACROPHAGE INNATE IMMUNE FUNCTION IN HIVR01HL063655 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KOZIEL, HENRY · 2000 to 2010
$4.1M
Alveolar macrophage NF-kB signaling in HIVF32HL071372 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ZHANG, JIANMIN · 2002 to 2004
$167k
NHLBI NIH HHS F32 HL071372NHLBI NIH HHS F32 HL71372NHLBI NIH HHS R01 HL063655NHLBI NIH HHS R01 HL63655
6 · The paper itself

Abstract

Alveolar macrophages (AM) represent important effector cells in the innate immune response to the AIDS-related pathogen Pneumocystis, but the early AM host defense signaling events are poorly defined. Using AM from healthy individuals, we showed in the present study that Pneumocystis organisms stimulate AM NF-kappaB p50 and p65 nuclear translocation in a time-dependent and multiplicity-of-infection-dependent manner as determined by electrophoretic mobility shift assay and immunofluorescence microscopy and that NF-kappaB nuclear translocation is associated with I-kappaB phosphorylation. Importantly, competitive inhibition of mannose receptor and targeted short interfering RNA-mediated gene suppression of mannose receptor mRNA and protein is associated with complete elimination of NF-kappaB nuclear translocation in response to Pneumocystis. Furthermore, human immunodeficiency virus (HIV) infection of AM (as a model human disease state of reduced AM mannose receptor expression and function) inhibits Pneumocystis-mediated NF-kappaB nuclear translocation and is associated with reduced I-kappaB phosphorylation and reduced interleukin-8 (IL-8) release. In contrast, NF-kappaB nuclear translocation and IL-8 release in response to lipopolysaccharide are intact in AM from both healthy and HIV-infected individuals, indicating that the observed impairment is not a global disturbance of the NF-kappaB pathway. Thus, in addition to phagocytic and endocytic effector functions, the present study identifies mannose receptors as pattern recognition receptors capable of NF-kappaB activation in response to infectious non-self challenge. AM mannose receptor-mediated NF-kappaB activation may represent an important mechanism of the host cell response to Pneumocystis, and altered NF-kappaB activation in the context of HIV infection may impair a critical innate immune signaling response and may contribute to pathogenesis of opportunistic lung infections.

Indexed as

Signal TransductionAdultAnimalsCell NucleusFemaleGene SilencingHIV-1HIV InfectionsHumansI-kappa B ProteinsLectins, C-TypeMacrophage ActivationMacrophages, AlveolarMaleMannose-Binding LectinsMannose ReceptorI-kappa B ProteinsLectins, C-TypeMannose-Binding LectinsMannose ReceptorNF-kappa BReceptors, Cell Surface

Identifiers

PMID15155616
PMCPMC415687
OpenAlexW2165572302

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.