Evidence map›Paper›PMID 22174452›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

The critical role of complement alternative pathway regulator factor H in allergen-induced airway hyperresponsiveness and inflammation.

Katsuyuki Takeda, Joshua M Thurman, Stephen Tomlinson, Masakazu Okamoto, Yoshiki Shiraishi, Viviana P Ferreira, Claudio Cortes, Michael K Pangburn, V Michael Holers, Erwin W Gelfand

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Article
  2. Article
  3. Effects ofEvidence-based complementary and alternative medicine : eCAM · 2020
    Article
  4. The relationship between complement C3 expression and the MUC5B genotype in pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2018
    Article
  5. Review
  6. Article
  7. Efficacy of Targeted Complement Inhibition in Experimental C3 Glomerulopathy.Journal of the American Society of Nephrology : JASN · 2016
    Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. 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

10 authors.

Katsuyuki TakedaDivision of Cell Biology, Department of Pediatrics, National Jewish Health, Denver, CO 80206, USA.
Joshua M Thurman
Stephen Tomlinson
Masakazu Okamoto
Yoshiki Shiraishi
Viviana P Ferreira
Claudio Cortes
Michael K Pangburn
V Michael Holers
Erwin W Gelfand

Funding

Signaling Memory in Chronic AsthmaP01HL036577 · NHLBI · NATIONAL JEWISH HEALTH · PI DAKHAMA, AZZEDDINE · 1986 to 2011
$18.7M
The Complement System and Ischemic Acute Renal FailureR01DK076690 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI Joshua M Thurman · 2008 to 2026
$6.6M
REGULATION OF COMPLEMENT BY MEMBRANE PROTEINSR01DK035081 · NIDDK · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI PANGBURN, MICHAEL K. · 1986 to 2011
$2.5M
Naturally Occurring T Regulatory Cells Control Airway HyperresponsivenessR01AI077609 · NIAID · NATIONAL JEWISH HEALTH · PI GELFAND, ERWIN WILLIAM · 2009 to 2013
$2.3M
RSV ENHANCES SENSITIZATION AND AIRWAY RESPONSIVENESSR01HL061005 · NHLBI · NATIONAL JEWISH HEALTH · PI GELFAND, ERWIN WILLIAM · 1999 to 2007
$2.2M
Naturally occurring T regulatory cells control airway hyperresponsivenessR56AI077609 · NIAID · NATIONAL JEWISH HEALTH · PI GELFAND, ERWIN WILLIAM · 2008 to 2008
$487k
ACTIVATION OF THE ALTERNATIVE PATHWAY OF COMPLEMENTR37DK035081 · NIDDK · UNIVERSITY OF TEXAS HLTH CTR AT TYLER · PI PANGBURN, MICHAEL K. · 1993 to 2000
$206k
NHLBI NIH HHS HL-36577NHLBI NIH HHS HL-61005NHLBI NIH HHS P01 HL036577NHLBI NIH HHS R01 HL061005NIAID NIH HHS AI-77609NIAID NIH HHS R01 AI077609NIAID NIH HHS R56 AI077609NIDDK NIH HHS DK-35081NIDDK NIH HHS R01 DK035081NIDDK NIH HHS R01 DK076690NIDDK NIH HHS R37 DK035081
6 · The paper itself

Abstract

Activation of the alternative pathway of complement plays a critical role in the development of allergen-induced airway hyperresponsiveness (AHR) and inflammation in mice. Endogenous factor H, a potent inhibitor of the alternative pathway, is increased in the airways of sensitized and challenged mice, but its role in regulating inflammation or AHR has been unknown. We found that blocking the tissue-binding function of factor H with a competitive antagonist increased complement activation and tissue inflammation after allergen challenge of sensitized mice. Conversely, administration of a fusion protein that contains the iC3b/C3d binding region of complement receptor 2 linked to the inhibitory region of factor H, a molecule directly targeting complement-activating surfaces, protected mice in both primary and secondary challenge models of AHR and lung inflammation. Thus, although endogenous factor H does play a role in limiting the development of AHR, strategies to deliver the complement-regulatory region of factor H specifically to the site of inflammation provide greater protection than that afforded by endogenous regulators. Such an agent may be an effective therapy for the treatment of asthma.

Indexed as

AllergensAnimalsAsthmaBronchial HyperreactivityComplement Factor HComplement Pathway, AlternativeFemaleInflammationInflammation MediatorsMiceMice, Inbred C57BLOvalbuminAllergensComplement Factor HInflammation MediatorsOvalbumin

Identifiers

PMID22174452
PMCPMC3253223

What OpenQuestion holds

Textmetadata
LicenceTDM
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.