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Cells
Special Issues
Fibrosis in Chronic Inflammatory Diseases
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Fibrosis in Chronic Inflammatory Diseases

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

Deadline for manuscript submissions: 25 December 2024 | Viewed by 1531

Special Issue Editors

Prof. Dr. Mirko Manetti

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Guest Editor
Department of Experimental and Clinical Medicine, Section of Anatomy and Histology, University of Florence, Largo Brambilla 3, 50134 Florence, Italy
Interests: anatomy; histology; morphological and functional aspects of stromal cells; endothelial cell biology; angiogenesis; cellular and molecular mechanisms of tissue fibrosis; pathogenesis of autoimmune, chronic inflammatory and connective tissue diseases; animal models of human disorders; systemic sclerosis; scleroderma
Special Issues, Collections and Topics in MDPI journals
Dr. Irene Rosa

E-Mail Website
Guest Editor
Department of Experimental and Clinical Medicine, Section of Anatomy and Histology, University of Florence, Largo Brambilla 3, 50134 Florence, Italy
Interests: anatomy; histology; morphological and functional aspects of stromal cells and endothelial cells; angiogenesis; tissue fibrosis; systemic sclerosis; scleroderma
Special Issues, Collections and Topics in MDPI journals
Dr. Eloisa Romano

E-Mail Website
Guest Editor
Department of Experimental and Clinical Medicine, Division of Rheumatology, University of Florence, Largo Brambilla 3, 50134 Florence, Italy
Interests: angiogenesis; cellular and molecular mechanisms of tissue fibrosis; pathogenesis of autoimmune diseases; chronic inflammatory and connective tissue diseases; systemic sclerosis; scleroderma; endothelial cell biology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are very glad to announce a Special Issue entitled "Fibrosis in Chronic Inflammatory Diseases" that is being prepared for publication in Cells.

Fibrosis, or scarring, is defined by the overgrowth and hardening of tissues due to excess synthesis and deposition of extracellular matrix components. When highly progressive, fibrosis leads to organ dysfunction, accounting for an increasingly large fraction of morbidity and mortality worldwide. In most cases, fibrosis is the end result of chronic inflammation induced by a variety of stimuli such as persistent infections, autoimmune reactions, allergic responses, chemical insults, radiation and tissue injury of different etiologies.

Over the last decade, knowledge regarding the pathophysiology of tissue fibrosis has advanced considerably. A feature common to all fibrotic diseases is the differentiation of extracellular matrix-producing myofibroblasts, which are persistently activated by various profibrotic mechanisms, including paracrine signals derived from inflammatory/immune cells and autocrine factors. Moreover, it is now clear that myofibroblasts can be generated from different cellular sources such as tissue-resident fibroblasts, mesenchymal stromal cells, adipocytes, epithelial and endothelial cells, as well as bone marrow-derived circulating precursors. Significant recent advancements also include the demonstration of common profibrotic molecular pathways across organs, namely transforming growth factor-β, Wnt and hedgehog signaling, among others. Nevertheless, there are still major challenges in the quest to develop effective antifibrotic therapeutic strategies. Indeed, it also appears that the transition from the inflammatory insult to fibrosis and the mechanisms progressing fibrosis may be either common or tissue/disease-specific. Therefore, a deeper understanding of the cellular and molecular mechanisms underlying fibrosis and its relationship with the inflammatory process is necessary to identify new therapeutic targets and increase treatment possibilities.

Outstanding experts interested in this Special Issue are very welcome to submit original manuscripts and reviews dealing with any aspects of the pathogenesis and pathophysiology of fibrosis in chronic inflammatory diseases.

Prof. Dr. Mirko Manetti
Dr. Irene Rosa
Dr. Eloisa Romano
Guest Editors

Dr. Bianca Saveria Fioretto
Guest Editor Assistant

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • fibrosis
  • fibroblasts
  • myofibroblasts
  • inflammation
  • molecular pathways
  • pathogenetic mechanisms
  • therapeutic targets

Published Papers (3 papers)

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17 pages, 15081 KiB  
Article
Fibrogenesis in Human Mucosa and Muscularis Precision-Cut Intestinal Slices
by Carin Biel, Anniek Kastermans, Janneke Heidema, Martin Pehrsson, Charlotte Henstra, Joachim Mortensen, Klaas Nico Faber and Peter Olinga
Cells 2024, 13(13), 1084; https://doi.org/10.3390/cells13131084 - 22 Jun 2024
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Abstract
In Crohn’s Disease (CD), intestinal fibrosis is a prevalent yet unresolved complication arising from chronic and transmural inflammation. The histological assessment of CD intestines shows changes in tissue morphology in all the layers, including the mucosa and muscularis. This study aimed to determine [...] Read more.
In Crohn’s Disease (CD), intestinal fibrosis is a prevalent yet unresolved complication arising from chronic and transmural inflammation. The histological assessment of CD intestines shows changes in tissue morphology in all the layers, including the mucosa and muscularis. This study aimed to determine the differences in fibrogenesis between mucosa and muscularis. Human precision-cut intestinal slices (hPCIS) were prepared from human intestine mucosa and muscularis and treated with TGF-β1 and/or PDGF-BB for 72 h. Gene and protein expression and matrix metalloproteinase (MMP) activity were determined. The basal gene expression of various fibrosis markers was higher in muscularis compared to mucosa hPCIS. During incubation, Pro-Collagen-1A1 secretion increased in muscularis but not in mucosa hPCIS. MMP gene expression increased during incubation in mucosa and muscularis hPCIS, except for MMP9, MMP12, and MMP13 in muscularis hPCIS. Incubation with TGF-β1 caused increased COL1A1 expression in the mucosa but not in muscularis hPCIS. In muscularis hPCIS, TGF-β1 treatment caused a decrease in MMP1 and CTSK expression, while MMP13 was increased. In the presence of TGF-β1, protease inhibitor expression was stable, except for SERPINE1, which was increased in muscularis hPCIS. We conclude that fibrogenesis is more pronounced in muscularis hPCIS compared to mucosa hPCIS, especially when stimulated with TGF-β1. Full article
(This article belongs to the Special Issue Fibrosis in Chronic Inflammatory Diseases)
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17 pages, 8441 KiB  
Article
Blockade of Sialylation with Decrease in Polysialic Acid Levels Counteracts Transforming Growth Factor β1-Induced Skin Fibroblast-to-Myofibroblast Transition
by Bianca Saveria Fioretto, Irene Rosa, Alessia Tani, Elena Andreucci, Eloisa Romano, Eleonora Sgambati and Mirko Manetti
Cells 2024, 13(12), 1067; https://doi.org/10.3390/cells13121067 - 19 Jun 2024
Viewed by 562
Abstract
Aberrant sialylation with overexpression of the homopolymeric glycan polysialic acid (polySia) was recently reported in fibroblasts from fibrotic skin lesions. Yet, whether such a rise in polySia levels or sialylation in general may be functionally implicated in profibrotic activation of fibroblasts and their [...] Read more.
Aberrant sialylation with overexpression of the homopolymeric glycan polysialic acid (polySia) was recently reported in fibroblasts from fibrotic skin lesions. Yet, whether such a rise in polySia levels or sialylation in general may be functionally implicated in profibrotic activation of fibroblasts and their transition to myofibroblasts remains unknown. Therefore, we herein explored whether inhibition of sialylation could interfere with the process of skin fibroblast-to-myofibroblast transition induced by the master profibrotic mediator transforming growth factor β1 (TGFβ1). Adult human skin fibroblasts were pretreated with the competitive pan-sialyltransferase inhibitor 3-Fax-peracetyl-Neu5Ac (3-Fax) before stimulation with recombinant human TGFβ1, and then analyzed for polySia expression, cell viability, proliferation, migratory ability, and acquisition of myofibroblast-like morphofunctional features. Skin fibroblast stimulation with TGFβ1 resulted in overexpression of polySia, which was effectively blunted by 3-Fax pre-administration. Pretreatment with 3-Fax efficiently lessened TGFβ1-induced skin fibroblast proliferation, migration, changes in cell morphology, and phenotypic and functional differentiation into myofibroblasts, as testified by a significant reduction in FAP, ACTA2, COL1A1, COL1A2, and FN1 gene expression, and α-smooth muscle actin, N-cadherin, COL1A1, and FN-EDA protein levels, as well as a reduced contractile capability. Moreover, skin fibroblasts pre-administered with 3-Fax displayed a significant decrease in Smad3-dependent canonical TGFβ1 signaling. Collectively, our in vitro findings demonstrate for the first time that aberrant sialylation with increased polySia levels has a functional role in skin fibroblast-to-myofibroblast transition and suggest that competitive sialyltransferase inhibition might offer new therapeutic opportunities against skin fibrosis. Full article
(This article belongs to the Special Issue Fibrosis in Chronic Inflammatory Diseases)
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7 pages, 945 KiB  
Brief Report
The Novel Cytokine Interleukin-41/Meteorin-like Is Reduced in Diffuse Systemic Sclerosis
by Paul Freedman, Bettina Schock and Steven O’Reilly
Cells 2024, 13(14), 1205; https://doi.org/10.3390/cells13141205 (registering DOI) - 17 Jul 2024
Abstract
Systemic sclerosis (SSc) is an autoimmune connective tissue disease with a triad of features that include vascular abnormalities, inflammation and skin and lung fibrosis. At the core of the disease is the activation of myofibroblasts from quiescent fibroblasts and this can be modified [...] Read more.
Systemic sclerosis (SSc) is an autoimmune connective tissue disease with a triad of features that include vascular abnormalities, inflammation and skin and lung fibrosis. At the core of the disease is the activation of myofibroblasts from quiescent fibroblasts and this can be modified by various cytokines. IL-41 is a recently described cytokine that was initially characterised as an adipokine as it was highly expressed in adipocytes and adipose tissue. However, it has recently been identified as being widely expressed and has immunomodulatory functions. This study examined the circulating levels of IL-41 and its expression in skin biopsies. We demonstrated significantly reduced levels of IL-41 in diffuse SSc that was also mirrored in the skin of SSc patients. AMPK has been proposed as a downstream target of IL-41, so we also measure mammalian target of rapamycin in skin and found that this is elevated in SSc patients. We speculate that IL-41 maybe an antifibrotic cytokine and its reduction may facilitate the activation of fibroblasts. Full article
(This article belongs to the Special Issue Fibrosis in Chronic Inflammatory Diseases)
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