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Review
. 2024 Aug 28;14(9):1080.
doi: 10.3390/biom14091080.

From Pathogenesis to Treatment: Targeting Type-2 Inflammation in Eosinophilic Esophagitis

Alberto Barchi  1   2 , Francesco Vito Mandarino  1 , Mona-Rita Yacoub  3 , Luca Albarello  4 , Luca Massimino  1 , Edoardo Vincenzo Savarino  5   6 , Federica Ungaro  1 , Sandro Passaretti  1 , Gwen M C Masclee  2 , Silvio Danese  1   7 , Albert J Bredenoord  2 , Edoardo Vespa  1
Affiliations
Review

From Pathogenesis to Treatment: Targeting Type-2 Inflammation in Eosinophilic Esophagitis

Alberto Barchi et al. Biomolecules. .

Abstract

Eosinophilic esophagitis (EoE) is a chronic inflammatory disorder of the esophagus. EoE shares a common pathogenetic mechanism with other chronic disorders pertaining to the type 2 inflammatory spectrum, such as atopic dermatitis (AD), allergic rhinitis (AR), asthma, and chronic rhinosinusitis with nasal polyps (CRSwNP). The recent advancements in EoE pathogenesis understanding have unveiled new molecular targets implied within the "atopic march" picture as well as specific to EoE. These discoveries have led to the clinical evaluation of several novel drugs (monoclonal antibodies and immune modulators), specifically aimed at the modulation of Th2 inflammation. In this comprehensive review, we have focused on the subtle mechanisms of type 2 inflammatory disorders, highlighting the similarities and differences with EoE, taking a deeper look into the evolving field of biologic therapies, already approved or under current investigation.

Keywords: EoE; atopic march; atopy; biologics; eosinophilic esophagitis; type 2 inflammation.

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Conflict of interest statement

A.B., F.V.M., M.-R.Y., L.A., L.M., F.U., S.P., and G.M.C.M. have no conflicts of interest to declare related to this article. E.V.S. served as a consultant for Abbvie, Agave, Alfasigma, Biogen, Bristol Myers Squibb, Celltrion, Diadema Farmaceutici, Falk, Fenix Pharma, Fresenius Kabi, Janssen, J.B. Pharmaceuticals, Merck & Co, Nestlè, Reckitt Benckiser, Regeneron, Sanofi, SILA, Sofar, Synformulas GmbH, Takeda, and Unifarco; he received research support from Pfizer, Reckitt Benckiser, SILA, Sofar, Unifarco, and Zeta Farmaceutici. S.D. received consultancy fees from AbbVie, Alimentiv, Allergan, Amgen, AstraZeneca, Athos Therapeutics, Biogen, Boehringer Ingelheim, Celgene, Celltrion, Eli Lilly, Enthera, Ferring Pharmaceuticals Inc., Gilead, Hospira, Inotrem, Janssen, Johnson & Johnson, MSD, Mundipharma, Mylan, Pfizer, Roche, Sandoz, Sublimity Therapeutics, Takeda, TiGenix, UCB Inc., and Vifor. A.J.B. received research funding from Nutricia, Norgine, Thelial, SST, and Falk Pharma and received speaker and/or consulting fees from Laborie, Thelial, EsoCap, Medtronic, Falk Pharma, Calypso Biotech, Alimentiv, Sanofi/Regeneron, Reckett, and AstraZeneca, and E.V. received speaker and/or consulting fees from Sanofi/Regeneron, Falk Pharma, Apollo Therapeutics, and Aurora Biofarma.

Figures

Figure 1
Figure 1
Principal disorders related to type 2 inflammation with pivotal molecules implicated in Th2 immune response and leading biological mechanisms.
Figure 2
Figure 2
Molecular pathways within eosinophilic esophagitis (EoE) pathogenesis, displaying the most relevant molecular targets of novel biologic drugs addressing type 2 inflammatory drive.
See this image and copyright information in PMC

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