Evidence map›Paper›PMID 25525732›Full record

ReviewAnnals of the American Thoracic Society2014

Airway fibrinogenolysis and the initiation of allergic inflammation.

Valentine Ongeri Millien, Wen Lu, Garbo Mak, Xiaoyi Yuan, J Morgan Knight, Paul Porter, Farrah Kheradmand, David B Corry

Open access · greenAbstract readReview
In one paragraph

Review in Annals of the American Thoracic Society, 2014. 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
0.9field-weighted citation impact, top 25% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Hypoxia-inducible factor-dependent induction of myeloid-derived netrin-1 attenuates natural killer cell infiltration during endotoxin-induced lung injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  6. Article
  7. Article
  8. Article
  9. Fibrinogen Is a Specific Trigger for Cytolytic Eosinophil Degranulation.Journal of immunology (Baltimore, Md. : 1950) · 2020
    Article
  10. Review
  11. Plasma metabolite profiles in children with current asthma.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2018
    Article
  12. Article
  13. Review
  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

8 authors at 3 institutions in 2 countries.

Valentine Ongeri Millien1 Translational Biology and Molecular Medicine Program.
Wen Lu
Garbo Mak
Xiaoyi Yuan
J Morgan Knight
Paul Porter
Farrah Kheradmand
David B Corry
Baylor College of Medicine · USCenter for Translational Molecular Medicine · NLMichael E. DeBakey VA Medical Center · US

Funding

Initiative for Maximizing Student Development (IMSD) ProgramR25GM056929 · NIGMS · BAYLOR COLLEGE OF MEDICINE · PI PEREIRA, FRED A · 1998 to 2023
$12.4M
The Role of Proteinases in Experimental AsthmaU19AI070973 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI EISSA, N. TONY · 2006 to 2010
$6.7M
Training Program in Translational Biology and Molecular MedicineT32GM088129 · NIGMS · BAYLOR COLLEGE OF MEDICINE · PI ROONEY, CLIONA M., VAN DEN VEYVER, IGNATIA B · 2010 to 2019
$3.0M
Molecular Phenotypes for Lung DiseasesR01HL095382 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI CORRY, DAVID B, KHERADMAND, FARRAH · 2008 to 2011
$2.8M
Adhesion Molecules in Allergic Lung InflammationR01AI057696 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI CORRY, DAVID B · 2005 to 2009
$1.6M
Th1 and Th17 Mediators in Experimental EmphysemaR01HL117181 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI CORRY, DAVID B, KHERADMAND, FARRAH · 2013 to 2016
$1.5M
Airway Epithelial Control of Allergic Lung InflammationK02HL075243 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI CORRY, DAVID B · 2004 to 2008
$506k
Carbon Black Induced Activation of Lung APCsI01BX002221 · VA · MICHAEL E DEBAKEY VA MEDICAL CENTER · PI CORRY, DAVID B · 2013 to 2016
–
BLRD VA I01 BX002221NHLBI NIH HHS HL75243NHLBI NIH HHS K02 HL075243NHLBI NIH HHS R01 HL095382NHLBI NIH HHS R01 HL117181NIAID NIH HHS AI057696NIAID NIH HHS AI070973NIAID NIH HHS R01 AI057696NIAID NIH HHS U19 AI070973NIGMS NIH HHS R25 GM056929NIGMS NIH HHS R25GM56929NIGMS NIH HHS T32 GM088129NIGMS NIH HHS T32GM088129
6 · The paper itself

Abstract

The past 15 years of allergic disease research have produced extraordinary improvements in our understanding of the pathogenesis of airway allergic diseases such as asthma. Whereas it was previously viewed as largely an immunoglobulin E-mediated process, the gradual recognition that T cells, especially Type 2 T helper (Th2) cells and Th17 cells, play a major role in asthma and related afflictions has inspired clinical trials targeting cytokine-based inflammatory pathways that show great promise. What has yet to be clarified about the pathogenesis of allergic inflammatory disorders, however, are the fundamental initiating factors, both exogenous and endogenous, that drive and sustain B- and T-cell responses that underlie the expression of chronic disease. Here we review how proteinases derived from diverse sources drive allergic responses. A central discovery supporting the proteinase hypothesis of allergic disease pathophysiology is the role played by airway fibrinogen, which in part appears to serve as a sensor of unregulated proteinase activity and which, when cleaved, both participates in a novel allergic signaling pathway through Toll-like receptor 4 and forms fibrin clots that contribute to airway obstruction. Unresolved at present is the ultimate source of airway allergenic proteinases. From among many potential candidates, perhaps the most intriguing is the possibility such enzymes derive from airway fungi. Together, these new findings expand both our knowledge of allergic disease pathophysiology and options for therapeutic intervention.

Indexed as

Immunity, CellularAllergensAsthmaCytokinesFibrinogenHumansHypersensitivityInflammationRespiratory SystemTh2 CellsAllergensCytokinesFibrinogenasthmafibrinogenproteolysissinusitisTh2 cells

Identifiers

PMID25525732
PMCPMC4298970
OpenAlexW2162246420

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.