Evidence map›Paper›PMID 28583447›Full record

ReviewThe Journal of allergy and clinical immunology2017

Etiology of epithelial barrier dysfunction in patients with type 2 inflammatory diseases.

Robert P Schleimer, Sergejs Berdnikovs

Abstract readReview
In one paragraph

Review in The Journal of allergy and clinical immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed, 1 pooled it
–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

96 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Therapeutic responses toScience translational medicine · 2020
    Trial
  3. Monoclonal Antibodies in Pediatric Atopic Dermatitis; Efficacy and Safety.Current therapeutic research, clinical and experimental · 2026
    Review
  4. Article
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  20. Early-Life Allergen Exposure and Its Influence on Risk of Atopic Disease.The journal of allergy and clinical immunology. In practice · 2025
    Review

36 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

2 authors.

Robert P SchleimerDivision of Allergy and Immunology, Northwestern University Feinberg School of Medicine, Chicago, Ill.
Sergejs BerdnikovsDivision of Allergy and Immunology, Northwestern University Feinberg School of Medicine, Chicago, Ill. Electronic address: s-berdnikovs@northwestern.edu.

Funding

Systems Genetics Approach to Gene Discovery in Chronic RhinosinusitisU19AI106683 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI KERN, ROBERT C · 2014 to 2017
$7.9M
Glucocorticosteroid Action In Inflammatory DiseaseR37HL068546 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SCHLEIMER, ROBERT P · 2009 to 2018
$3.5M
Hormones in allergic diseaseR01AI127783 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BERDNIKOVS, SERGEJS · 2017 to 2021
$2.0M
Novel asthma pathogenesis genes in the mucosa of the human airwaysR21AI115055 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BERDNIKOVS, SERGEJS · 2015 to 2016
$425k
NHLBI NIH HHS R37 HL068546NIAID NIH HHS R01 AI127783NIAID NIH HHS R21 AI115055NIAID NIH HHS U19 AI106683
6 · The paper itself

Abstract

Epithelial barriers of the skin, gastrointestinal tract, and airway serve common critical functions, such as maintaining a physical barrier against environmental insults and allergens and providing a tissue interface balancing the communication between the internal and external environments. We now understand that in patients with allergic disease, regardless of tissue location, the homeostatic balance of the epithelial barrier is skewed toward loss of differentiation, reduced junctional integrity, and impaired innate defense. Importantly, epithelial dysfunction characterized by these traits appears to pre-date atopy and development of allergic disease. Despite our growing appreciation of the centrality of barrier dysfunction in initiation of allergic disease, many important questions remain to be answered regarding mechanisms disrupting normal barrier function. Although our external environment (proteases, allergens, and injury) is classically thought of as a principal contributor to barrier disruption associated with allergic sensitization, there is a need to better understand contributions of the internal environment (hormones, diet, and circadian clock). Systemic drivers of disease, such as alterations of the endocrine system, metabolism, and aberrant control of developmental signaling, are emerging as new players in driving epithelial dysfunction and allergic predisposition at various barrier sites. Identifying such central mediators of epithelial dysfunction using both systems biology tools and causality-driven laboratory experimentation will be essential in building new strategic interventions to prevent or reverse the process of barrier loss in allergic patients.

Indexed as

AnimalsEpitheliumHumansHypersensitivityInflammationallergic predispositionallergic sensitizationdifferentiationEpithelial barrierextracellular matrixhormonesmesenchymemetabolismtight junctions

Identifiers

PMID28583447
PMCPMC5753806

What OpenQuestion holds

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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.