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Author Spotlight: Investigating the Pathophysiology of Eosinophilic Esophagitis
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Elements Involved In Promoting Eosinophilic Gastrointestinal Disorders.

Anshi Shukla1, Akanksha Mishra1, Sathisha Upparahalli Venkateshaiah1

  • 1Department of Medicine, Section of Pulmonary Diseases, Tulane Eosinophilic Disorder Center, 1430 Tulane Avenue, New Orleans, LA 70112.

Journal of Genetic Syndromes & Gene Therapy
|November 15, 2016
PubMed
Summary
This summary is machine-generated.

Eosinophilic gastrointestinal disorders (EGID) involve eosinophil buildup in the digestive tract. Targeting iNKT cells shows promise for new diagnostics and therapies for these food allergen-induced conditions.

Keywords:
EGEEGIDEoEEosinophilsFood allergyInterleukiniNKT cells

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Area of Science:

  • Immunology
  • Gastroenterology
  • Allergy

Background:

  • Eosinophilic gastrointestinal disorders (EGID) are food allergen-induced conditions characterized by eosinophil accumulation in the GI tract.
  • EGID encompasses eosinophilic esophagitis (EoE), gastritis (EG), gastroenteritis (EGE), and colitis (EC), with complex and not fully understood pathogenesis.
  • Current diagnostic methods rely on invasive endoscopic and histopathological evaluations, lacking reliable noninvasive biomarkers.

Purpose of the Study:

  • To review key elements in EGID initiation, progression, and pathogenesis.
  • To highlight the need for novel noninvasive diagnostic biomarkers for EGID.
  • To explore iNKT cells as a potential therapeutic target for EGID.

Main Methods:

  • Review of existing literature on EGID pathogenesis, including cytokine and cellular involvement.
  • Analysis of current diagnostic and therapeutic strategies for EGID.
  • Discussion of emerging research on iNKT cells in EGID models.

Main Results:

  • Specific cytokines (IL-4, IL-5, IL-13, IL-15, IL-18, eotaxins) are implicated in EGID pathogenesis.
  • Current therapies like antigen elimination and corticosteroids are effective, but cytokine-targeted therapies (anti-IL-5, anti-IL-13) have shown limited success in EoE.
  • iNKT cells are identified as key producers of eosinophil-active cytokines and are implicated in EoE pathogenesis, with neutralization showing protective effects in experimental models.

Conclusions:

  • EGID pathogenesis is complex, involving multiple cytokines and cellular players.
  • There is a critical need for noninvasive diagnostic biomarkers and more effective therapies for EGID.
  • Targeting iNKT cells presents a promising avenue for future diagnostic and therapeutic interventions in EGID.