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Cells
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Mucosal Immunity and Epithelial Barrier Biology: From Tissue Homeostasis to...
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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: closed (20 September 2024) | Viewed by 5004

Special Issue Editors

Prof. Dr. Charles Pilette

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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
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Marie Baeck

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Guest Editor
Department of Dermatology, Cliniques Universitaires Saint-Luc, Université Catholique de Louvain, Brussels, Belgium
Interests: dermatology; allergology; immunology
Prof. Dr. Peter Stärkel

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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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Keywords

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

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Published Papers (4 papers)

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Research

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18 pages, 19371 KiB  
Article
The Barrier Disruption and Pyroptosis of Intestinal Epithelial Cells Caused by Perfringolysin O (PFO) from Clostridium perfringens
by Zhankui Liu, Shuang Mou, Liang Li, Qichao Chen, Ruicheng Yang, Shibang Guo, Yancheng Jin, Lixinjie Liu, Tianzhi Li, Huanchun Chen and Xiangru Wang
Cells 2024, 13(13), 1140; https://doi.org/10.3390/cells13131140 - 3 Jul 2024
Viewed by 1335
Abstract
Clostridium perfringens (C. perfringens), a Gram-positive bacterium, produces a variety of toxins and extracellular enzymes that can lead to disease in both humans and animals. Common symptoms include abdominal swelling, diarrhea, and intestinal inflammation. Severe cases can result in complications like [...] Read more.
Clostridium perfringens (C. perfringens), a Gram-positive bacterium, produces a variety of toxins and extracellular enzymes that can lead to disease in both humans and animals. Common symptoms include abdominal swelling, diarrhea, and intestinal inflammation. Severe cases can result in complications like intestinal hemorrhage, edema, and even death. The primary toxins contributing to morbidity in C. perfringens-infected intestines are CPA, CPB, CPB2, CPE, and PFO. Amongst these, CPB, CPB2, and CPE are implicated in apoptosis development, while CPA is associated with cell death, increased intracellular ROS levels, and the release of the inflammatory factor IL-18. However, the exact mechanism by which PFO toxins exert their effects in the infected gut is still unidentified. This study demonstrates that a C. perfringens PFO toxin infection disrupts the intestinal epithelial barrier function through in vitro and in vivo models. This study emphasizes the notable influence of PFO toxins on intestinal barrier integrity in the context of C. perfringens infections. It reveals that PFO toxins increase ROS production by causing mitochondrial damage, triggering pyroptosis in IPEC-J2 cells, and consequently resulting in compromised intestinal barrier function. These results offer a scientific foundation for developing preventive and therapeutic approaches against C. perfringens infections. Full article
(This article belongs to the Special Issue Mucosal Immunity and Epithelial Barrier Biology: From Tissue Homeostasis to Chronic Disease)
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22 pages, 3013 KiB  
Article
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; https://doi.org/10.3390/cells13090760 - 29 Apr 2024
Viewed by 1762
Abstract
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
(This article belongs to the Special Issue Mucosal Immunity and Epithelial Barrier Biology: From Tissue Homeostasis to Chronic Disease)
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Review

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20 pages, 1991 KiB  
Review
Mucosal Inflammatory Memory in Chronic Rhinosinusitis
by Min-Seok Koo, Sungmin Moon and Min-Seok Rha
Cells 2024, 13(23), 1947; https://doi.org/10.3390/cells13231947 - 23 Nov 2024
Viewed by 250
Abstract
Recent advancements in medical management, endoscopic sinus surgery, and biologics have significantly improved outcomes for patients with chronic rhinosinusitis (CRS). However, long-term recurrence is frequently observed following endoscopic sinus surgery, with symptoms worsening after biologics are discontinued. Consequently, refractory or recurrent CRS remains [...] Read more.
Recent advancements in medical management, endoscopic sinus surgery, and biologics have significantly improved outcomes for patients with chronic rhinosinusitis (CRS). However, long-term recurrence is frequently observed following endoscopic sinus surgery, with symptoms worsening after biologics are discontinued. Consequently, refractory or recurrent CRS remains a significant challenge, causing a substantial healthcare burden. In this review, we provide current insights into mucosal inflammatory memory, a potential mechanism leading to CRS recurrence. Given that both immune and non-immune cells in the sinonasal mucosa play critical roles in the pathophysiology of CRS, a deeper understanding of the mechanisms underlying mucosal inflammatory memory in various cellular components of sinonasal tissue could aid in the management of refractory CRS. We describe and discuss the latest knowledge regarding the novel concept of inflammatory memory, including both adaptive immune memory and trained immunity. Additionally, we summarize the pathogenic memory features of the sinonasal mucosa cellular components in the context of CRS. Full article
(This article belongs to the Special Issue Mucosal Immunity and Epithelial Barrier Biology: From Tissue Homeostasis to Chronic Disease)

Other

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11 pages, 2302 KiB  
Brief Report
Nanoparticle Uptake in the Aging and Oncogenic Drosophila Midgut Measured with Surface-Enhanced Raman Spectroscopy
by Maria Christou, Ayobami Fidelix, Yiorgos Apidianakis and Chrysafis Andreou
Cells 2024, 13(16), 1344; https://doi.org/10.3390/cells13161344 - 13 Aug 2024
Viewed by 1133
Abstract
Colorectal cancer remains a major global health concern. Colonoscopy, the gold-standard colorectal cancer diagnostic, relies on the visual detection of lesions and necessitates invasive biopsies for confirmation. Alternative diagnostic methods, based on nanomedicine, can facilitate early detection of malignancies. Here, we examine the [...] Read more.
Colorectal cancer remains a major global health concern. Colonoscopy, the gold-standard colorectal cancer diagnostic, relies on the visual detection of lesions and necessitates invasive biopsies for confirmation. Alternative diagnostic methods, based on nanomedicine, can facilitate early detection of malignancies. Here, we examine the uptake of surface-enhanced Raman scattering nanoparticles (SERS NPs) as a marker for intestinal tumor detection and imaging using an established Drosophila melanogaster model for gut disease. Young and old Oregon-R and w1118 flies were orally administered SERS NPs and scanned without and upon gut lumen clearance to assess nanoparticle retention as a function of aging. Neither young nor old flies showed significant NP retention in their body after gut lumen clearance. Moreover, tumorigenic flies of the esg-Gal4/UAS-RasV12 genotype were tested for SERS NP retention 2, 4 and 6 days after RasV12 oncogene induction in their midgut progenitor cells. Tumorigenic flies showed a statistically significant NP retention signal at 2 days, well before midgut epithelium impairment. The signal was then visualized in scans of dissected guts revealing areas of NP uptake in the posterior midgut region of high stem cell activity. Full article
(This article belongs to the Special Issue Mucosal Immunity and Epithelial Barrier Biology: From Tissue Homeostasis to Chronic Disease)
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