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Cytokines and Chemokines: Modulators of Epithelial Cell Biology in Health and Disease

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A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Medical Biology".

Deadline for manuscript submissions: closed (15 October 2022) | Viewed by 11235

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Special Issue Editors

Prof. Dr. Barry James Campbell

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Guest Editor

Gastroenterology Research Unit, Department of Infection Biology & Microbiomes, Institute of Infection, Veterinary and Ecological Sciences, Faculty of Health & Life Sciences, University of Liverpool, Liverpool L69 3GE, UK
Interests: gut secretory cell biology; epithelial glycobiology; bacteria-host interaction in inflammation and cancer; intestinal microbiota

Dr. Stamatia Papoutsopoulou

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Guest Editor

Department of Biochemistry & Biotechnology, University of Thessaly, 41500 Larissa, Greece
Interests: innate immunity; mucosa immunity; transcription factor pathways; IBD; Parkinson’s
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Dear Colleagues,

It is well established that epithelial surfaces are responsible for protection, in the intestine for absorption of nutrients and prevention of inflammatory conditions induced by exogenous factors, such as the associated microbiota, and foreign and/or dietary antigens. This is achieved by maintenance of a physical barrier, synthesis of a mucus layer, secretion of antimicrobial peptides and active engagement in immune cell regulation to facilitate the internalisation, processing and efﬁcient presentation of antigens. Cytokines and chemokines can have pro- and anti-inflammatory actions and can positively or negatively affect epithelial cell proliferation, cell death and barrier permeability. During inflammation and/or cancer, there is an increased mobilisation and activation of immune cells, the barrier integrity is compromised and there is an increasing tissue destruction. Chemokines that belong to a constitutive or homeostatic group mostly play an important role in the development and organisation of associated lymphoid tissue. On the other hand, inducible chemokines and cytokines are secreted in a response to proinflammatory signals and play a crucial role in epithelial inflammation and its resolution, and their dysregulation has been linked to stress, infection, inflammatory disease, cancer and inflammation-associated damage.

In this Special Issue, we propose highlighting recent advances in our understanding of how cytokines and chemokines, both those made by and those acting on the epithelium, orchestrate many of the diverse functions of the different specialised epithelial cell types and their interactions with cells of the innate immune system (such as dendritic cells, macrophages, monocytes and neutrophils), both in health and disease.

We welcome manuscripts particularly focused on the intrinsic role of epithelial cell-derived cytokines and chemokines, as this is an area that is still poorly understood.

Prof. Dr. Barry James Campbell
Dr. Stamatia Papoutsopoulou
Guest Editors

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Keywords

cytokine
chemokine
epithelium
mucosal immunology
epithelial homeostasis
infection
stress
inflammation and cancer

Published Papers (4 papers)

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14 pages, 2063 KiB

Open AccessArticle

Interleukin-10 Deficiency Impacts on TNF-Induced NFκB Regulated Responses In Vivo

by Stamatia Papoutsopoulou, Liam Pollock, Jonathan M. Williams, Maya M. L. F. Abdul-Mahdi, Reyhaneh Dobbash, Carrie A. Duckworth and Barry J. Campbell

Biology 2022, 11(10), 1377; https://0-doi-org.brum.beds.ac.uk/10.3390/biology11101377 - 20 Sep 2022

Viewed by 2002

Abstract

Interleukin-10 (IL-10) is an anti-inflammatory cytokine that has a major protective role against intestinal inflammation. We recently revealed that intestinal epithelial cells in vitro regulate NFκB-driven transcriptional responses to TNF via an autocrine mechanism dependent on IL-10 secretion. Here in this study, we investigated the impact of IL-10 deficiency on the NFκB pathway and its downstream targets in the small intestinal mucosa in vivo. We observed dysregulation of TNF, IκBα, and A20 gene and protein expression in the small intestine of steady-state or TNF-injected Il10^−/− mice, compared to wild-type C57BL6/J counterparts. Upon TNF injection, tissue from the small intestine showed upregulation of NFκB p65[RelA] activity, which was totally diminished in Il10^−/− mice and correlated with reduced levels of TNF, IκBα, and A20 expression. In serum, whilst IgA levels were noted to be markedly downregulated in IL-10-deficient^- mice, normal levels of mucosal IgA were seen in intestine mucosa. Importantly, dysregulated cytokine/chemokine levels were observed in both serum and intestinal tissue lysates from naïve, as well as TNF-injected Il10^−/− mice. These data further support the importance of the IL-10-canonical NFκB signaling pathway axis in regulating intestinal mucosa homeostasis and response to inflammatory triggers in vivo. Full article

(This article belongs to the Special Issue Cytokines and Chemokines: Modulators of Epithelial Cell Biology in Health and Disease)

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17 pages, 34538 KiB

Open AccessArticle

Epithelial-Mesenchymal Plasticity Induced by Discontinuous Exposure to TGFβ1 Promotes Tumour Growth

by Mafalda Santos, Marta Ferreira, Patrícia Oliveira, Nuno Mendes, Ana André, André F. Vieira, Joana B. Nunes, Joana Carvalho, Sara Rocha, Mafalda Azevedo, Daniel Ferreira, Inês Reis, João Vinagre, Joana Paredes, Alireza Heravi-Moussavi, Jorge Lima, Valdemar Máximo, Angela Burleigh, Calvin Roskelley, Fátima Carneiro, David Huntsman and Carla Oliveira Show full author list Hide full author list

Biology 2022, 11(7), 1046; https://0-doi-org.brum.beds.ac.uk/10.3390/biology11071046 - 12 Jul 2022

Cited by 3 | Viewed by 1796

Abstract

Transitions between epithelial and mesenchymal cellular states (EMT/MET) contribute to cancer progression. We hypothesize that EMT followed by MET promotes cell population heterogeneity, favouring tumour growth. We developed an EMT model by on and off exposure of epithelial EpH4 cells (E-cells) to TGFβ1 that mimics phenotypic EMT (M-cells) and MET. We aimed at understanding whether phenotypic MET is accompanied by molecular and functional reversion back to epithelia by using RNA sequencing, immunofluorescence (IF), proliferation, wound healing, focus formation and mamosphere formation assays as well as cell xenografts in nude mice. Phenotypic reverted epithelial cells (RE-cells) obtained after MET induction presented epithelial morphologies and proliferation rates resembling E cells. However, the RE transcriptomic profile and IF staining of epithelial and mesenchymal markers revealed a uniquely heterogeneous mixture of cell subpopulations with a high self-renewal ability. RE cell heterogeneity was stably maintained for long periods after TGFβ1 removal both in vitro and in large tumours derived from the nude mice. Overall, we show that phenotypic reverted epithelial cells (RE cells) do not return to the molecular and functional epithelial state and present mesenchymal features related to aggressiveness and cellular heterogeneity that favour tumour growth in vivo. This work strengthens epithelial cell reprogramming and cellular heterogeneity fostered by inflammatory cues as a tumour growth-promoting factor in vivo. Full article

(This article belongs to the Special Issue Cytokines and Chemokines: Modulators of Epithelial Cell Biology in Health and Disease)

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16 pages, 1519 KiB

Open AccessArticle

Interleukin-27 Regulates the Function of the Gastrointestinal Epithelial Barrier in a Human Tissue-Derived Organoid Model

by Daniel P. Brice, Graeme I. Murray, Heather M. Wilson, Ross J. Porter, Susan Berry, Scott K. Durum and Mairi H. McLean

Biology 2022, 11(3), 427; https://0-doi-org.brum.beds.ac.uk/10.3390/biology11030427 - 11 Mar 2022

Cited by 6 | Viewed by 3541

Abstract

A treatment with direct healing effects on the gastrointestinal epithelial barrier is desirable for inflammatory bowel disease (IBD). Interleukin-27 (IL-27) is an immunoregulatory cytokine, and oral delivery is an effective treatment in murine models of IBD. We aimed to define IL-27 effects on the human gastrointestinal epithelial barrier. We characterised gene and protein expression of permeability mediators in a human colon-derived organoid model. Functional permeability was determined in an organoid-derived 2D monolayer by transepithelial electrical resistance. IL-27 effects on epithelial innate immune responses were assessed through expression of cytokines, anti-microbial peptides and MUC genes. IL-27 effects on wound healing and proliferation were determined in human colon epithelial cell lines. IL-27 led to restoration of permeability regulation following inflammatory cytokine insult (p = 0.001), associated with differential expression of tight junction mediators with decrease in claudin 2 (p = 0.024) and increase in claudin 4 (p < 0.001), E-cadherin (p < 0.001) and zona occludens (p = 0.0014). IL-27 evoked differential gene expression of epithelial-derived innate immune responses (reduced IL1B and IL18, and increased IL33, HBD1, MUC1 and MUC2; p < 0.012). IL-27 induced epithelial barrier wound healing through restitution (p < 0.001), and increased proliferation (p < 0.001) following injury. Overall, IL-27 provokes mucosal healing of the human gastrointestinal epithelial barrier. Full article

(This article belongs to the Special Issue Cytokines and Chemokines: Modulators of Epithelial Cell Biology in Health and Disease)

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13 pages, 935 KiB

Open AccessSystematic Review

Parkinson’s Disease, It Takes Guts: The Correlation between Intestinal Microbiome and Cytokine Network with Neurodegeneration

by Georgia Xiromerisiou, Chrysoula Marogianni, Anastasia Androutsopoulou, Panagiotis Ntavaroukas, Dimitrios Mysiris and Stamatia Papoutsopoulou

Biology 2023, 12(1), 93; https://0-doi-org.brum.beds.ac.uk/10.3390/biology12010093 - 07 Jan 2023

Cited by 2 | Viewed by 3063

Abstract

Parkinson’s disease is a progressive neurodegenerative disorder with motor, physical and behavioral symptoms that can have a profound impact on the patient’s quality of life. Most cases are idiopathic, and the exact mechanism of the disease’s cause is unknown. The current hypothesis focuses on the gut-brain axis and states that gut microbiota dysbiosis can trigger inflammation and advances the development of Parkinson’s disease. This systematic review presents the current knowledge of gut microbiota analysis and inflammation based on selected studies on Parkinson’s patients and experimental animal models. Changes in gut microbiota correlate with Parkinson’s disease, but only a few studies have considered inflammatory modulators as important triggers of the disease. Nevertheless, it is evident that proinflammatory cytokines and chemokines are induced in the gut, the circulation, and the brain before the development of the disease’s neurological symptoms and exacerbate the disease. Increased levels of tumor necrosis factor, interleukin-1β, interleukin-6, interleukin-17A and interferon-γ can correlate with altered gut microbiota. Instead, treatment of gut dysbiosis is accompanied by reduced levels of inflammatory mediators in specific tissues, such as the colon, brain and serum and/or cerebrospinal fluid. Deciphering the role of the immune responses and the mechanisms of the PD-associated gut microbiota will assist the interpretation of the pathogenesis of Parkinson’s and will elucidate appropriate therapeutic strategies. Full article

(This article belongs to the Special Issue Cytokines and Chemokines: Modulators of Epithelial Cell Biology in Health and Disease)

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