Comparative Transcriptomics of IBD Patients Indicates Induction of Type 2 Immunity Irrespective of the Disease Ideotype

Gonzalez Acera M, Patankar J, Diemand L, Siegmund B, Neurath M, Wirtz S, Becker C (2021)

Publication Type: Journal article

Publication year: 2021

Journal

Frontiers in Medicine Frontiers Media

Book Volume: 8

Article Number: 664045

DOI: 10.3389/fmed.2021.664045

Abstract

Inflammatory cytokines initiate and sustain the perpetuation of processes leading to chronic inflammatory conditions such as inflammatory bowel diseases (IBD). The nature of the trigger causing an inflammatory reaction decides whether type 1, type 17, or type 2 immune responses, typically characterized by the respective T- helper cell subsets, come into effect. In the intestine, Type 2 responses have been linked with mucosal healing and resolution upon an immune challenge involving parasitic infections. However, type 2 cytokines are frequently elevated in certain types of IBD in particular ulcerative colitis (UC) leading to the assumption that Th2 cells might critically support the pathogenesis of UC raising the question of whether such elevated type 2 responses in IBD are beneficial or detrimental. In line with this, previous studies showed that suppression of IL-13 and other type 2 related molecules in murine models could improve the outcomes of intestinal inflammation. However, therapeutic attempts of neutralizing IL-13 in ulcerative colitis patients have yielded no benefits. Thus, a better understanding of the role of type 2 cytokines in regulating intestinal inflammation is required. Here, we took a comparative transcriptomic approach to address how Th2 responses evolve in different mouse models of colitis and human IBD datasets. Our data show that type 2 immune-related transcripts are induced in the inflamed gut of IBD patients in both Crohn's disease and UC and across widely used mouse models of IBD. Collectively our data implicate that the presence of a type 2 signature rather defines a distinct state of intestinal inflammation than a disease-specific pathomechanism.

Authors with CRIS profile

Miguel Gonzalez Acera Department of Medicine 1 – Gastroenterology, Pneumology and Endocrinology Jay Patankar Department of Medicine 1 – Gastroenterology, Pneumology and Endocrinology Markus Neurath Lehrstuhl für Innere Medizin I (Medizin 1) Stefan Wirtz Department of Medicine 1 – Gastroenterology, Pneumology and Endocrinology Christoph Becker Professur für Molekulare Gastroenterologie

Additional Organisation(s)

Interdisziplinäres Zentrum für Klinische Forschung (IZKF)

Related research project(s)

A076: Elucidating the regulation and function of Gasdermin C in intestinal infection and inflammation Feb. 1, 2020 - Jan. 31, 2023

Involved external institutions

Charité - Universitätsmedizin Berlin DE Germany (DE)

How to cite

APA:

Gonzalez Acera, M., Patankar, J., Diemand, L., Siegmund, B., Neurath, M., Wirtz, S., & Becker, C. (2021). Comparative Transcriptomics of IBD Patients Indicates Induction of Type 2 Immunity Irrespective of the Disease Ideotype. Frontiers in Medicine, 8. https://doi.org/10.3389/fmed.2021.664045

MLA:

Gonzalez Acera, Miguel, et al. "Comparative Transcriptomics of IBD Patients Indicates Induction of Type 2 Immunity Irrespective of the Disease Ideotype." Frontiers in Medicine 8 (2021).

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