Evidence map›Paper›PMID 15723703›Full record

ReviewRespiratory research2005

Anaphylatoxin C3a receptors in asthma.

Hydar Ali, Reynold A Panettieri

Open access · goldAbstract readReview
In one paragraph

Review in Respiratory research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Deciphering the Intricate Roles of Radiation Therapy and Complement Activation in Cancer.International journal of radiation oncology, biology, physics · 2020
    Review
  6. Article
  7. Presence of positive skin prick tests to inhalant allergens and markers of T2 inflammation in subjects with chronic spontaneous urticaria (CSU): a systematic literature review.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2020
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Peanuts can contribute to anaphylactic shock by activating complement.The Journal of allergy and clinical immunology · 2009
    Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Hydar AliDepartment of Pathology, School of Dental Medicine, University of Pennsylvania, 240 South 40th Street, Philadelphia, PA 19104, USA. ali@path.dental.upenn.edu
Reynold A Panettieri
University of Pennsylvania · US

Funding

MECHANISMS REGULATING AIRWAY MUSCLE GROWTHR01HL055301 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI PANETTIERI, REYNOLD ALEXANDER · 1996 to 2003
$1.1M
G-PROTEIN COUPLED RECEPTORS IN ASTHMA AND INFLAMMATIONR01HL063372 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI ALI, HYDAR · 2000 to 2003
$1.1M
NHLBI NIH HHS 1R01-HL63372NHLBI NIH HHS 2R01-HL-55301NHLBI NIH HHS R01 HL055301NHLBI NIH HHS R01 HL063372
6 · The paper itself

Abstract

The complement system forms the central core of innate immunity but also mediates a variety of inflammatory responses. Anaphylatoxin C3a, which is generated as a byproduct of complement activation, has long been known to activate mast cells, basophils and eosinophils and to cause smooth muscle contraction. However, the role of C3a in the pathogenesis of allergic asthma remains unclear. In this review, we examine the role of C3a in promoting asthma. Following allergen challenge, C3a is generated in the lung of subjects with asthma but not healthy subjects. Furthermore, deficiency in C3a generation or in G protein coupled receptor for C3a abrogates allergen-induced responses in murine models of pulmonary inflammation and airway hyperresponsiveness. In addition, inhibition of complement activation or administration of small molecule inhibitors of C3a receptor after sensitization but before allergen challenge inhibits airway responses. At a cellular level, C3a stimulates robust mast cell degranulation that is greatly enhanced following cell-cell contact with airway smooth muscle (ASM) cells. Therefore, C3a likely plays an important role in asthma primarily by regulating mast cell-ASM cell interaction.

Indexed as

AnaphylatoxinsAnimalsAsthmaComplement C3aHumansMembrane ProteinsReceptors, ComplementAnaphylatoxinsComplement C3acomplement C3a receptorMembrane ProteinsReceptors, Complement

Identifiers

PMID15723703
PMCPMC551592
OpenAlexW2137706297

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.