Mucosal Immunity and Epithelial Barrier Biology: From Tissue Homeostasis to Chronic Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: 20 September 2024 | Viewed by 988

Special Issue Editors

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Guest Editor
Department of Respiratory Medicine, Cliniques Universitaires St-Luc, Institute of Experimental and Clinical Research, Université Catholique de Louvain (UCL), 10 Avenue Hippocrate, B-1200 Brussels, Belgium
Interests: mucosal immunology; respiratory medicine; allergy and pulmonary diseases; IgA; lung epithelium biology
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Guest Editor
Department of Dermatology, Cliniques Universitaires Saint-Luc, Université Catholique de Louvain, Brussels, Belgium
Interests: dermatology; allergology; immunology

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Guest Editor
1. Department of Hepato-Gastroenterology, Cliniques Universitaires Saint-Luc, Brussels, Belgium
2. Laboratory of Hepato-Gastroenterology, Institute of Experimental and Clinical Research, UCLouvain, Brussels, Belgium
Interests: gut immunity; intestinal epithelial barrier; intestinal immunity; hepatology; gastroenterology; alcoholology

Special Issue Information

Dear Colleagues,

The airways, from the nose to the deep pulmonary alveoli, the gut, and the skin are directly exposed to external matters, leading to a challenge for those epithelial barriers and the immune system to prevent unnecessary responses and to adapt their response to noxious or harmless exposures. Homeostasis at mucosal and skin barriers involves a complex interplay between structural and immune cells, an emerging concept being the “memory” of previous responses that is developed not only in immune cells but also in epithelial stem cells. Several diseases, such as chronic rhinosinusitis, asthma, colitis and allergic dermatitis are typically linked with aberrant cell responses to external matters. They share longstanding histories of repeated exposure-repair cycles over years that may cause alterations in organ development, epithelial-mesenchymal unit biology as well as chronic immune activation. Altered mucosal immunity (notably its major mediator, namely IgA) integrates the pathophysiology of such chronic diseases and could reflect an abnormal interplay with the gut/lung microbiome in chronic disease. Early dysregulation of mucosal barriers may also imprint barrier tissues during childhood to promote future disease development. The studies of mucosal and skin (dys)immunity that consider both cross-organ similarities and specificities, should provide in the future valuable targets for preventive or therapeutic interventions in order to tackle pathogenic mechanisms before irreversible changes feed the roots of chronic disease.

Prof. Dr. Charles Pilette
Prof. Dr. Marie Baeck
Prof. Dr. Peter Stärkel
Guest Editors

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  • epithelial barrier
  • mucosal immunity
  • immune system
  • skin barrier
  • skin immunity
  • IgA
  • chronic disease
  • airways
  • respiratory
  • lung
  • gut
  • skin
  • therapeutic interventions

Published Papers (1 paper)

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22 pages, 3013 KiB  
JAK/STAT Inhibition Normalizes Lipid Composition in 3D Human Epidermal Equivalents Challenged with Th2 Cytokines
by Enrica Flori, Alessia Cavallo, Sarah Mosca, Daniela Kovacs, Carlo Cota, Marco Zaccarini, Anna Di Nardo, Grazia Bottillo, Miriam Maiellaro, Emanuela Camera and Giorgia Cardinali
Cells 2024, 13(9), 760; - 29 Apr 2024
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Derangement of the epidermal barrier lipids and dysregulated immune responses are key pathogenic features of atopic dermatitis (AD). The Th2-type cytokines interleukin IL-4 and IL-13 play a prominent role in AD by activating the Janus Kinase/Signal Transduction and Activator of Transcription (JAK/STAT) intracellular [...] Read more.
Derangement of the epidermal barrier lipids and dysregulated immune responses are key pathogenic features of atopic dermatitis (AD). The Th2-type cytokines interleukin IL-4 and IL-13 play a prominent role in AD by activating the Janus Kinase/Signal Transduction and Activator of Transcription (JAK/STAT) intracellular signaling axis. This study aimed to investigate the role of JAK/STAT in the lipid perturbations induced by Th2 signaling in 3D epidermal equivalents. Tofacitinib, a low-molecular-mass JAK inhibitor, was used to screen for JAK/STAT-mediated deregulation of lipid metabolism. Th2 cytokines decreased the expression of elongases 1, 3, and 4 and serine-palmitoyl-transferase and increased that of sphingolipid delta(4)-desaturase and carbonic anhydrase 2. Th2 cytokines inhibited the synthesis of palmitoleic acid and caused depletion of triglycerides, in association with altered phosphatidylcholine profiles and fatty acid (FA) metabolism. Overall, the ceramide profiles were minimally affected. Except for most sphingolipids and very-long-chain FAs, the effects of Th2 on lipid pathways were reversed by co-treatment with tofacitinib. An increase in the mRNA levels of CPT1A and ACAT1, reduced by tofacitinib, suggests that Th2 cytokines promote FA beta-oxidation. In conclusion, pharmacological inhibition of JAK/STAT activation prevents the lipid disruption caused by the halted homeostasis of FA metabolism. Full article
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