Evidence map›Paper›PMID 19620403›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2009

Attenuation of IgG immune complex-induced acute lung injury by silencing C5aR in lung epithelial cells.

Lei Sun, Ren-Feng Guo, Hongwei Gao, J Vidya Sarma, Firas S Zetoune, Peter A Ward

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

35 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Immune Defense Protein Expression in Highly Purified Mouse Lung Epithelial Cells.American journal of respiratory cell and molecular biology · 2016
    Article
  17. Contribution of the anaphylatoxin receptors, C3aR and C5aR, to the pathogenesis of pulmonary fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Article
  18. Article
  19. Review
  20. Crosstalk between TGF-β1 and complement activation augments epithelial injury in pulmonary fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014
    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

6 authors at 2 institutions in 2 countries.

Lei SunDepartment of Pathology, University of Michigan Medical School, 1301 Catherine Rd., Ann Arbor, MI 48109-5602, USA.
Ren-Feng Guo
Hongwei Gao
J Vidya Sarma
Firas S Zetoune
Peter A Ward
University of Michigan–Ann Arbor · USMedizinische Hochschule Hannover · DE

Funding

MONONUCLEAR LEUKOCYTE ADHESION AND RECRUITMENT IN CHRONIC INFLAMMATORY DISEASEP01HL031963 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI JOHNSON, KENT JOHN · 1985 to 2009
$14.1M
Protective Effects of Anti-C5a in SepsisR01GM061656 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WARD, PETER A · 2002 to 2013
$3.8M
NHLBI NIH HHS HL-31963NHLBI NIH HHS P01 HL031963NIGMS NIH HHS GM-61656NIGMS NIH HHS R01 GM061656
6 · The paper itself

Abstract

Acute lung injury (ALI) in mouse lung occurs after distal airway deposition of IgG immune complexes (IgGICs), resulting in a breakdown of the vascular-airway barrier, causing intrapulmonary edema, hemorrhage, and accumulation of neutrophils [polymorphonuclear leukocytes (PMNs)] in the alveolar compartment, these changes being complement (C5a) and C5a receptor (C5aR) dependent. In this ALI model, C5aR expression (protein) was found to occur on upper (bronchial) and lower (alveolar) airway epithelial cells. An adenovirus construct (siRNA) was used to silence mRNA for C5aR in the lung. Under such conditions, C5aR protein was markedly reduced on lung epithelial cells, resulting in much reduced leakage of albumin into the lung, diminished buildup of PMNs, and lower levels of proinflammatory mediators in bronchoalveolar lavage fluids. These studies indicate that bronchial and alveolar epithelial cell C5aR is up-regulated and greatly contributes to inflammation and injury in the lung. The use of siRNA administered into the airways avoids systemic suppression of C5aR, which might compromise innate immunity. It is possible that such an intervention might be employed in humans with ALI or acute respiratory distress syndrome as well as in upper-airway inflammatory diseases, such as chronic obstructive pulmonary disease and asthma, where there is evidence for complement activation and buildup of PMNs.

Indexed as

RNA InterferenceAcute Lung InjuryAnimalsAntigen-Antibody ComplexBronchiComplement C5aEpithelial CellsImmunoglobulin GMaleMiceMice, Inbred C57BLPeroxidasePulmonary AlveoliReceptor, Anaphylatoxin C5aRNA, Small InterferingAntigen-Antibody ComplexComplement C5aImmunoglobulin GPeroxidaseReceptor, Anaphylatoxin C5aRNA, Small Interfering

Identifiers

PMID19620403
PMCPMC2775006
OpenAlexW2092967574

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.