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Mast Cells and Fibrosis

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (18 June 2021) | Viewed by 15549

Special Issue Editor


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Guest Editor
Robert C. Byrd Health Sciences Center, 64 Medical Center Drive, West Virginia University, Morgantown, WV, USA
Interests: fibrosis; inflammation; neuropeptides
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Mast cells (MCs) are non-circulating immune cells that develop only when bone marrow-derived precursors have reached their target tissue. These tissue MCs then go through several stages of maturation driven primarily by the c-kit ligand, a stem cell factor, with the final MC phenotype being highly dependent on the microenvironment in which they reside. While mast cells are classically linked to allergic reactions, particularly anaphylaxis, these cells also contribute to other processes within the body—some beneficial and some detrimental. Accumulating evidence suggests that mast cells are important in promoting fibrosis in numerous organs. This Special Issue on “Mast Cells and Fibrosis” welcomes submissions that both support a pro-fibrotic role for mast cells as well as evidence against mast cells being pro-fibrotic, and the studies can relate to any organ.

Dr. Scott Levick
Guest Editor

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.

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Published Papers (4 papers)

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Research

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24 pages, 5770 KiB  
Article
Sex-Specific Effects of Plastic Caging in Murine Viral Myocarditis
by Katelyn A. Bruno, Logan P. Macomb, A. Carolina Morales-Lara, Jessica E. Mathews, J. Augusto Frisancho, Alex L. Yang, Damian N. Di Florio, Brandy H. Edenfield, Emily R. Whelan, Gary R. Salomon, Anneliese R. Hill, Chathuranga C. Hewa-Rahinduwage, Ashley J. Scott, Henry D. Greyner, Frank A. Molina, Merci S. Greenaway, George M. Cooper and DeLisa Fairweather
Int. J. Mol. Sci. 2021, 22(16), 8834; https://doi.org/10.3390/ijms22168834 - 17 Aug 2021
Cited by 6 | Viewed by 3383
Abstract
Background: Myocarditis is an inflammatory heart disease caused by viral infections that can lead to heart failure, and occurs more often in men than women. Since animal studies have shown that myocarditis is influenced by sex hormones, we hypothesized that endocrine disruptors, which [...] Read more.
Background: Myocarditis is an inflammatory heart disease caused by viral infections that can lead to heart failure, and occurs more often in men than women. Since animal studies have shown that myocarditis is influenced by sex hormones, we hypothesized that endocrine disruptors, which interfere with natural hormones, may play a role in the progression of the disease. The human population is exposed to the endocrine disruptor bisphenol A (BPA) from plastics, such as water bottles and plastic food containers. Methods: Male and female adult BALB/c mice were housed in plastic versus glass caging, or exposed to BPA in drinking water versus control water. Myocarditis was induced with coxsackievirus B3 on day 0, and the endpoints were assessed on day 10 post infection. Results: We found that male BALB/c mice that were exposed to plastic caging had increased myocarditis due to complement activation and elevated numbers of macrophages and neutrophils, whereas females had elevated mast cell activation and fibrosis. Conclusions: These findings show that housing mice in traditional plastic caging increases viral myocarditis in males and females, but using sex-specific immune mechanisms. Full article
(This article belongs to the Special Issue Mast Cells and Fibrosis )
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16 pages, 3035 KiB  
Article
Crosstalk between Mast Cells and Lung Fibroblasts Is Modified by Alveolar Extracellular Matrix and Influences Epithelial Migration
by Mariam Bagher, Oskar Rosmark, Linda Elowsson Rendin, Annika Nybom, Sebastian Wasserstrom, Catharina Müller, Xiao-Hong Zhou, Göran Dellgren, Oskar Hallgren, Leif Bjermer, Anna-Karin Larsson-Callerfelt and Gunilla Westergren-Thorsson
Int. J. Mol. Sci. 2021, 22(2), 506; https://doi.org/10.3390/ijms22020506 - 6 Jan 2021
Cited by 10 | Viewed by 3354
Abstract
Mast cells play an important role in asthma, however, the interactions between mast cells, fibroblasts and epithelial cells in idiopathic pulmonary fibrosis (IPF) are less known. The objectives were to investigate the effect of mast cells on fibroblast activity and migration of epithelial [...] Read more.
Mast cells play an important role in asthma, however, the interactions between mast cells, fibroblasts and epithelial cells in idiopathic pulmonary fibrosis (IPF) are less known. The objectives were to investigate the effect of mast cells on fibroblast activity and migration of epithelial cells. Lung fibroblasts from IPF patients and healthy individuals were co-cultured with LAD2 mast cells or stimulated with the proteases tryptase and chymase. Human lung fibroblasts and mast cells were cultured on cell culture plastic plates or decellularized human lung tissue (scaffolds) to create a more physiological milieu by providing an alveolar extracellular matrix. Released mediators were analyzed and evaluated for effects on epithelial cell migration. Tryptase increased vascular endothelial growth factor (VEGF) release from fibroblasts, whereas co-culture with mast cells increased IL-6 and hepatocyte growth factor (HGF). Culture in scaffolds increased the release of VEGF compared to culture on plastic. Migration of epithelial cells was reduced by IL-6, while HGF and conditioned media from scaffold cultures promoted migration. In conclusion, mast cells and tryptase increased fibroblast release of mediators that influenced epithelial migration. These data indicate a role of mast cells and tryptase in the interplay between fibroblasts, epithelial cells and the alveolar extracellular matrix in health and lung disease. Full article
(This article belongs to the Special Issue Mast Cells and Fibrosis )
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Review

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11 pages, 270 KiB  
Review
Mast Cell Involvement in Fibrosis in Chronic Graft-Versus-Host Disease
by Ethan Strattan and Gerhard Carl Hildebrandt
Int. J. Mol. Sci. 2021, 22(5), 2385; https://doi.org/10.3390/ijms22052385 - 27 Feb 2021
Cited by 6 | Viewed by 3438
Abstract
Allogeneic hematopoietic stem cell transplantation (HSCT) is most commonly a treatment for inborn defects of hematopoiesis or acute leukemias. Widespread use of HSCT, a potentially curative therapy, is hampered by onset of graft-versus-host disease (GVHD), classified as either acute or chronic GVHD. While [...] Read more.
Allogeneic hematopoietic stem cell transplantation (HSCT) is most commonly a treatment for inborn defects of hematopoiesis or acute leukemias. Widespread use of HSCT, a potentially curative therapy, is hampered by onset of graft-versus-host disease (GVHD), classified as either acute or chronic GVHD. While the pathology of acute GVHD is better understood, factors driving GVHD at the cellular and molecular level are less clear. Mast cells are an arm of the immune system that are known for atopic disease. However, studies have demonstrated that they can play important roles in tissue homeostasis and wound healing, and mast cell dysregulation can lead to fibrotic disease. Interestingly, in chronic GVHD, aberrant wound healing mechanisms lead to pathological fibrosis, but the cellular etiology driving this is not well-understood, although some studies have implicated mast cells. Given this novel role, we here review the literature for studies of mast cell involvement in the context of chronic GVHD. While there are few publications on this topic, the papers excellently characterized a niche for mast cells in chronic GVHD. These findings may be extended to other fibrosing diseases in order to better target mast cells or their mediators for treatment of fibrotic disease. Full article
(This article belongs to the Special Issue Mast Cells and Fibrosis )
21 pages, 2143 KiB  
Review
A Review of the Evidence for and against a Role for Mast Cells in Cutaneous Scarring and Fibrosis
by Traci A. Wilgus, Sara Ud-Din and Ardeshir Bayat
Int. J. Mol. Sci. 2020, 21(24), 9673; https://doi.org/10.3390/ijms21249673 - 18 Dec 2020
Cited by 29 | Viewed by 4401
Abstract
Scars are generated in mature skin as a result of the normal repair process, but the replacement of normal tissue with scar tissue can lead to biomechanical and functional deficiencies in the skin as well as psychological and social issues for patients that [...] Read more.
Scars are generated in mature skin as a result of the normal repair process, but the replacement of normal tissue with scar tissue can lead to biomechanical and functional deficiencies in the skin as well as psychological and social issues for patients that negatively affect quality of life. Abnormal scars, such as hypertrophic scars and keloids, and cutaneous fibrosis that develops in diseases such as systemic sclerosis and graft-versus-host disease can be even more challenging for patients. There is a large body of literature suggesting that inflammation promotes the deposition of scar tissue by fibroblasts. Mast cells represent one inflammatory cell type in particular that has been implicated in skin scarring and fibrosis. Most published studies in this area support a pro-fibrotic role for mast cells in the skin, as many mast cell-derived mediators stimulate fibroblast activity and studies generally indicate higher numbers of mast cells and/or mast cell activation in scars and fibrotic skin. However, some studies in mast cell-deficient mice have suggested that these cells may not play a critical role in cutaneous scarring/fibrosis. Here, we will review the data for and against mast cells as key regulators of skin fibrosis and discuss scientific gaps in the field. Full article
(This article belongs to the Special Issue Mast Cells and Fibrosis )
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