Evidence map›Paper›PMID 20238140›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2010

Effects of alpha 1-antitrypsin on endotoxin-induced lung inflammation in vivo.

Devipriya Subramaniyam, Chad Steele, Thomas Köhnlein, Tobias Welte, Olof Grip, Sadis Matalon, Sabina Janciauskiene

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 34 citations in OpenAlex.

  1. Case Report:Frontiers in immunology · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Alpha-1-antitrypsin monotherapy reduces graft-versus-host disease after experimental allogeneic bone marrow transplantation.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  14. Article
  15. Article
  16. 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

7 authors at 3 institutions in 3 countries.

Devipriya SubramaniyamDepartment of Respiratory Medicine, Hannover Medical School, Germany.
Chad Steele
Thomas Köhnlein
Tobias Welte
Olof Grip
Sadis Matalon
Sabina Janciauskiene
Medizinische Hochschule Hannover · DEUniversity of Alabama at Birmingham · USLund University · SE

Funding

PATHOPHYSIOLOGY OF SUBLETHAL OXYGEN IN INJURED LUNGSR01HL031197 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MARK N GILLESPIE, Sadis Matalon · 1985 to 2026
$4.2M
RSV infections augment Cl2 induced injury to the respiratory systemU54ES017218 · NIEHS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MATALON, SADIS · 2008 to 2011
$3.6M
Prevention and Treatment of Chlorine Gas Induced Injury to the Pulmonary SystemU01ES015676 · NIEHS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MATALON, SADIS · 2006 to 2011
$3.3M
NHLBI NIH HHS R01 HL031197NIEHS NIH HHS U01 ES015676NIEHS NIH HHS U54 ES017218
6 · The paper itself

Abstract

OBJECTIVE AND

designPrevious in vitro experiments demonstrated that acute-phase protein, alpha 1-antitrypsin (AAT), could act either as an enhancer or as a suppressor of lipopolysaccharide (LPS)-induced cell activation depending on treatment time. Here we investigate how AAT regulates inflammatory responses in the short term when administrated post LPS challenge.

methodsSimilar experimental setup was used both in vitro and in vivo: human monocytes and neutrophils were stimulated with LPS for 2 h followed by AAT for a total time of 4 h, and C57BL/6 mice were treated intranasally with LPS and 2 h later with AAT and sacrificed after 4 h. Bronchial lavage (BAL) and lung homogenates were analyzed using bio-plex cytokine assay. BAL cell counts were assessed.

resultsWithin 4 h, AAT enhanced LPS-induced tumor necrosis factor-alpha (TNFalpha), interleukin (IL)-6, and IL-8 release from monocytes and neutrophils. Mice challenged for 4 h with LPS followed by AAT at 2 h showed no changes in BAL cell counts and higher levels of almost all measured cytokines, specifically RANTES in BAL and IL-12, IL-13, granulocyte colony-stimulating factor (G-CSF), granulocyte macrophage colony-stimulating factor (GM-CSF), and IL-10 levels in lung homogenates, than in mice treated with LPS only.

conclusionWithin the short term, AAT enhances the magnitude of LPS-induced specific cytokine/chemokine production, which may play an important role in amplification and resolution of acute-phase inflammatory reactions in vivo.

Indexed as

alpha 1-AntitrypsinAnimalsBronchoalveolar Lavage FluidCells, CulturedCytokinesHumansInterleukin-6Interleukin-8LipopolysaccharidesLungMiceMice, Inbred C57BLMonocytesNeutrophilsPneumoniaTumor Necrosis Factor-alphaalpha 1-AntitrypsinCytokinesInterleukin-6Interleukin-8LipopolysaccharidesTumor Necrosis Factor-alpha

Identifiers

PMID20238140
OpenAlexW2067598698

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.