Evidence map›Paper›PMID 29879991›Full record

ReviewRespiratory research2018

Is IgE or eosinophils the key player in allergic asthma pathogenesis? Are we asking the right question?

Andrea Matucci, Alessandra Vultaggio, Enrico Maggi, Ismail Kasujee

Open access · goldAbstract readReview
In one paragraph

Review in Respiratory research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
14.1field-weighted citation impact, top 1% 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

87 citing papers in PubMed, 199 citations in OpenAlex.

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  15. IgG Antibody Titers AgainstTropical medicine and infectious disease · 2024
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27 more citing papers are in PubMed but not listed here.

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

4 authors at 3 institutions in 2 countries.

Andrea MatucciImmunoallergology Unit, Azienda Ospedaliero-Universitaria Careggi, Largo Brambilla 3, 50134, Florence, Italy. andrea.matucci@unifi.it.
Alessandra VultaggioImmunoallergology Unit, Azienda Ospedaliero-Universitaria Careggi, Largo Brambilla 3, 50134, Florence, Italy.
Enrico MaggiCenter for Research, Transfer and High Education DENOTHE, University of Florence, Florence, Italy.
Ismail KasujeeNovartis Pharma AG, Basel, Switzerland.
Azienda Ospedaliero-Universitaria Careggi · ITNovartis (Switzerland) · CHUniversity of Florence · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bronchial asthma (BA) is a chronic inflammatory disease with a marked heterogeneity in pathophysiology and etiology. The heterogeneity of BA may be related to the inducing mechanism(s) (allergic vs non-allergic), the histopathological background (eosinophilic vs non-eosinophilic), and the clinical manifestations, particularly in terms of severity and frequency of exacerbations. Asthma can be divided into at least two different endotypes based on the degree of Th2 inflammation (T2 'high' and T2 'low'). For patients with severe uncontrolled asthma, monoclonal antibodies (mAbs) against immunoglobulin E (IgE) or interleukin (IL)-5 are now available as add-on treatments. Treatment decisions for individual patients should consider the biological background in terms of the "driving mechanisms" of inflammation as this should predict the patients' likely responses to treatment. The question is not whether an anti-IgE or an anti-eosinophilic strategy is more effective, but rather what the mechanism is at the origin of the airway. While IgE is involved early in the inflammatory cascade and can be considered as a cause of allergic asthma, eosinophilia can be considered a consequence of the whole process. This article discusses the different roles of the IgE and IL-5/eosinophil pathways in the pathogenic mechanisms of airway inflammation occurring in allergic asthma, and the possible reasons to choose an anti-IgE mAb or anti-IL-5 treatment.

Indexed as

AnimalsAsthmaEosinophiliaEosinophilsHumansImmunoglobulin EInflammation MediatorsImmunoglobulin EInflammation MediatorsAnti-IL-5Asthma pathogenesis; anti-IgEEosinophilIgEIL-5Immunoglobulin EInterleukin 5

Identifiers

PMID29879991
PMCPMC5992661
OpenAlexW2805490366

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.