Evidence map›Paper›PMID 27840774›Full record

ArticleJournal of genetic syndromes & gene therapy2015

Elements Involved In Promoting Eosinophilic Gastrointestinal Disorders.

Anshi Shukla, Akanksha Mishra, Sathisha Upparahalli Venkateshaiah, Murli Manohar, Chandrashekara Puthanapura Mahadevappa, Anil Mishra

Open access · greenAbstract read
In one paragraph

Article in Journal of genetic syndromes & gene therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

7 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
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  6. Review
  7. Food-Induced Acute Pancreatitis.Digestive diseases and sciences · 2017
    Review
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

6 authors at 1 institution in 1 country.

Anshi ShuklaDepartment of Medicine, Section of Pulmonary Diseases, Tulane Eosinophilic Disorder Center, 1430 Tulane Avenue, New Orleans, LA 70112.
Akanksha MishraDepartment of Medicine, Section of Pulmonary Diseases, Tulane Eosinophilic Disorder Center, 1430 Tulane Avenue, New Orleans, LA 70112.
Sathisha Upparahalli VenkateshaiahDepartment of Medicine, Section of Pulmonary Diseases, Tulane Eosinophilic Disorder Center, 1430 Tulane Avenue, New Orleans, LA 70112.
Murli ManoharDepartment of Medicine, Section of Pulmonary Diseases, Tulane Eosinophilic Disorder Center, 1430 Tulane Avenue, New Orleans, LA 70112.
Chandrashekara Puthanapura MahadevappaDepartment of Medicine, Section of Pulmonary Diseases, Tulane Eosinophilic Disorder Center, 1430 Tulane Avenue, New Orleans, LA 70112.
Anil MishraDepartment of Medicine, Section of Pulmonary Diseases, Tulane Eosinophilic Disorder Center, 1430 Tulane Avenue, New Orleans, LA 70112.
Tulane University · US

Funding

Role of IL-15 in the Pathogensis of Eosinophilic EsophagitisR01AI080581 · NIAID · TULANE UNIVERSITY OF LOUISIANA · PI MISHRA, ANIL · 2009 to 2023
$4.9M
Mechanistic Analysis of Eosinophilic Esophagitis.R01DK067255 · NIDDK · TULANE UNIVERSITY OF LOUISIANA · PI MISHRA, ANIL · 2005 to 2014
$2.6M
NIAID NIH HHS R01 AI080581NIDDK NIH HHS R01 DK067255
6 · The paper itself

Abstract

Eosinophilic gastrointestinal disorders (EGID) are food allergen-induced allergic gastrointestinal disorders, characterized by accumulation of highly induced eosinophils in different segments of gastrointestinal tract along with eosinophil microabssess and extracellular eosinophilic granules in the epithelial layer. EGID are both IgE- and cell-mediated group of diseases that include eosinophilic esophagitis (EoE), eosinophilic gastritis (EG), eosinophilic gastroenteritis (EGE) and eosinophilic colitis (EC). Despite the increased incidences and considerable progress made in understanding EGID pathogenesis. The mechanism is still not well understood. It has been shown that IL-4, IL-5, IL-13, IL-15, IL-18, eotaxin-1, eotaxin-2 and eotaxin-3 play a critical role in EGID pathogenesis. Currently, the only criterion for diagnosing EoE, EGE and EC are repetitive endoscopic and histopathological evaluation of biopsies along with other clinical characteristics/manifestations. Antigen elimination and corticosteroid therapies are the most effective therapies currently in practice for the treatment of EGID. The cytokines (anti-IL-5 and anti-IL-13) therapy trials were not very successful in case of EoE. Most recently, a clinical trial using anti-IL-13 reported only 60% reduced esophageal eosinophilia without achieving primary endpoint. This clinical finding is not surprising and is in accordance with our earlier report indicating that IL-13 is not critical in the initiation of EoE. Notably, EGID still has no reliable noninvasive diagnostic biomarkers. Hence, there is a great necessity to identify novel noninvasive diagnostic biomarkers that can easily diagnose EGID and provide an effective therapy. Now, the attention is required to target cell types like iNKT cells that produce eosinophil active cytokines and is found induced in the pathogenesis of both experimental and human EoE. iNKT cell neutralization is shown to protect allergen-induced EoE in experimental model. In this review, we have discussed the key elements that are critical in the disease initiation, progression, pathogenesis and important for future diagnostic and therapeutic interventions for EGID.

Indexed as

EGEEGIDEoEEosinophilsFood allergyiNKT cellsInterleukin

Identifiers

PMID27840774
PMCPMC5102338
OpenAlexW2509906389

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.