Evidence map›Paper›PMID 22363629›Full record

ArticlePloS one2012

Intravenous immunoglobulin prevents murine antibody-mediated acute lung injury at the level of neutrophil reactive oxygen species (ROS) production.

John W Semple, Michael Kim, Jing Hou, Mark McVey, Young Jin Lee, Arata Tabuchi, Wolfgang M Kuebler, Zhong-Wei Chai, Alan H Lazarus

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 57 citations in OpenAlex.

  1. Transfusion-Related Acute Lung Injury: from Mechanistic Insights to Therapeutic Strategies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  2. Dysregulation of neutrophil in sepsis: recent insights and advances.Cell communication and signaling : CCS · 2025
    Review
  3. IgG hexamers initiate acute lung injury.bioRxiv : the preprint server for biology · 2024
    Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. The ATP-gated P2XScientific reports · 2019
    Article
  13. The Pathogenic Involvement of Neutrophils in Acute Respiratory Distress Syndrome and Transfusion-Related Acute Lung Injury.Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie · 2018
    Review
  14. Article
  15. Skeletal muscle regeneration is modulated by inflammation.Journal of orthopaedic translation · 2018
    Review
  16. Article
  17. Article
  18. Review
  19. Article
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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 3 institutions in 1 country.

John W SempleThe Toronto Platelet Immunobiology Group, University of Toronto, Toronto, Ontario, Canada. semplej@smh.ca
Michael Kim
Jing Hou
Mark McVey
Young Jin Lee
Arata Tabuchi
Wolfgang M Kuebler
Zhong-Wei Chai
Alan H Lazarus
St. Michael's Hospital · CAUniversity of Toronto · CACanadian Blood Services · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Transfusion-related acute lung injury (TRALI) is a leading cause of transfusion-associated mortality that can occur with any type of transfusion and is thought to be primarily due to donor antibodies activating pulmonary neutrophils in recipients. Recently, a large prospective case controlled clinical study of cardiac surgery patients demonstrated that despite implementation of male donors, a high incidence of TRALI still occurred and suggested a need for additional interventions in susceptible patient populations. To examine if intravenous immunoglobulin (IVIg) may be effective, a murine model of antibody-mediated acute lung injury that approximates human TRALI was examined. When BALB/c mice were injected with the anti-major histocompatibility complex class I antibody 34-1-2s, mild shock (reduced rectal temperature) and respiratory distress (dyspnea) were observed and pre-treatment of the mice with 2 g/kg IVIg completely prevented these symptoms. To determine IVIg's usefulness to affect severe lung damage, SCID mice, previously shown to be hypersensitive to 34-1-2s were used. SCID mice treated with 34-1-2s underwent severe shock, lung damage (increased wet/dry ratios) and 40% mortality within 2 hours. Treatment with 2 g/kg IVIg 18 hours before 34-1-2s administration completely protected the mice from all adverse events. Treatment with IVIg after symptoms began also reduced lung damage and mortality. While the prophylactic IVIg administration did not affect 34-1-2s-induced pulmonary neutrophil accumulation, bone marrow-derived neutrophils from the IVIg-treated mice displayed no spontaneous ROS production nor could they be stimulated in vitro with fMLP or 34-1-2s. These results suggest that IVIg prevents murine antibody-mediated acute lung injury at the level of neutrophil ROS production and thus, alleviating tissue damage.

Indexed as

AcidsAcute Lung InjuryAnimalsChemokine CXCL2EdemaHumansHypothermiaImmunoglobulins, IntravenousLungMaleMiceMice, Inbred BALB CMice, SCIDNeutrophilsReactive Oxygen SpeciesSurvival AnalysisAcidsChemokine CXCL2Cxcl2 protein, mouseImmunoglobulins, IntravenousReactive Oxygen Species

Identifiers

PMID22363629
PMCPMC3281967
OpenAlexW2064029287

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.