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OSM/OSMR and Interleukin 6 Family Cytokines in Physiological and Pathological Condition 2.0

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 (15 May 2023) | Viewed by 5767

Special Issue Editor

Dr. Francesca Lantieri

E-Mail Website
Guest Editor
Dipartimento di Scienze della Salute, Sezione di Biostatistica, Università degli Studi di Genova, 16132 Genoa, Italy
Interests: the study of human diseases through the statistical analysis of the biological and genetical data and in particular the dissection of the genetics of complex diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The interleukin-6 family is a group of cytokines with shared signaling properties, among which IL-6, Oncostatin M (OSM), leukemia inhibitory factor (LIF), and IL-31. They bind to a gp130/OSM receptor (OSMR) heterodimer complex or to a gp130/LIF receptor (LIFR) complex, while IL-31 binds to the OSMR/IL-31 receptor (IL-31R) complex. The receptor binding triggers several signaling pathways, among which Jak/STAT, the Ras-MAPK, the PI 3-K-Akt, the p38, and JNK MAPK pathways.

Both OSM and OSMR have been implicated in a variety of biological functions, including cell growth, neuronal development, and inflammatory responses. Their role has been also reported in several inflammation-related diseases and cancers and their potential as a therapy target suggested.

This Special Issue aims to uncover every aspect of IL-6 family cytokines and in particular OSM and/or OSMR functioning and signaling cascade that might unravel their role in both physiological and pathological conditions.

Dr. Francesca Lantieri
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.

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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.

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Published Papers (3 papers)

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Research

17 pages, 6115 KiB  
Article
Oncostatin M Contributes to Airway Epithelial Cell Dysfunction in Chronic Rhinosinusitis with Nasal Polyps
by Florent Carsuzaa, Emilie Bequignon, Sophie Bartier, André Coste, Xavier Dufour, Matthieu Bainaud, Jean Claude Lecron, Bruno Louis, Stéphane Tringali, Laure Favot and Maxime Fieux
Int. J. Mol. Sci. 2023, 24(7), 6094; https://doi.org/10.3390/ijms24076094 - 23 Mar 2023
Cited by 2 | Viewed by 1440
Abstract
Chronic rhinosinusitis with nasal polyps (CRSwNP) is a typical type-2 inflammation involving several cytokines and is associated with epithelial cell dysfunction. Oncostatin M (OSM) (belonging to the interleukin(IL)-6 family) could be a key driver of epithelial barrier dysfunction. Therefore, we investigated the presence [...] Read more.
Chronic rhinosinusitis with nasal polyps (CRSwNP) is a typical type-2 inflammation involving several cytokines and is associated with epithelial cell dysfunction. Oncostatin M (OSM) (belonging to the interleukin(IL)-6 family) could be a key driver of epithelial barrier dysfunction. Therefore, we investigated the presence of OSM and IL-6 and the expression pattern of tight junctions (TJs) in the nasal tissue of CRSwNP patients and controls using reverse transcriptase quantitative polymerase chain reaction (RT-qPCR) and Western blotting. Then, their potential role in the epithelial barrier was evaluated in vitro in 27 different primary cultures of human nasal epithelial cells (HNECs) by measuring TJ expression and transepithelial electric resistance (TEER) with or without OSM or IL-6 (1, 10, and 100 ng/mL). The effect on ciliary beating efficiency was evaluated by high-speed videomicroscopy and on repair mechanisms with a wound healing model with or without OSM. OSM and IL-6 were both overexpressed, and TJ (ZO-1 and occludin) expression was decreased in the nasal polyps compared to the control mucosa. OSM (100 ng/mL) but not IL-6 induced a significant decrease in TJ expression, TEER, and ciliary beating efficiency in HNECs. After 24 h, the wound repair rate was significantly higher in OSM-stimulated HNECs at 100 ng/mL. These results suggest that OSM could become a new target for monoclonal antibodies. Full article
(This article belongs to the Special Issue OSM/OSMR and Interleukin 6 Family Cytokines in Physiological and Pathological Condition 2.0)
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16 pages, 3602 KiB  
Article
Interleukin-31 Receptor A Expression in the Dorsal Root Ganglion of Mice with Atopic Dermatitis
by Iwao Arai and Saburo Saito
Int. J. Mol. Sci. 2023, 24(2), 1047; https://doi.org/10.3390/ijms24021047 - 05 Jan 2023
Cited by 3 | Viewed by 1755
Abstract
Atopic dermatitis (AD) is a common skin disease caused by genetic and environmental factors. However, the mechanisms underlying AD development remain unclear. In this study, we examined the genetic factors contributing to the onset of itch-associated scratching in different strains of mice. Interleukin-31 [...] Read more.
Atopic dermatitis (AD) is a common skin disease caused by genetic and environmental factors. However, the mechanisms underlying AD development remain unclear. In this study, we examined the genetic factors contributing to the onset of itch-associated scratching in different strains of mice. Interleukin-31 (IL-31) induces severe scratching and dermatitis in mice. However, the site of action of IL-31 remains unclear. Cutaneous IL-31 and IL-31 receptor A (IL-31RA) mRNAs in the dorsal root ganglion (DRG) are expressed exclusively in the AD model, i.e., NC/Nga mice. Here we evaluated the effects of repeated administration of IL-31 on the scratching behavior in NC/Nga, BALB/c, and C57BL/6 mice. The results showed that repeated administration of IL-31 significantly increased itch-associated scratching (LLS) behavior in the three strains of mice. One hour after an intravenous IL-31 injection, BALB/c mice showed alloknesis-like behavior. Mite infestation and IL-31 administration triggered itchy skin, increased LLS counts and DRG neuronal IL-31RA expression, and eventually caused dermatitis. The dermatitis severity and LLS counts induced by mite infestation and IL-31 administration were in the order NC/Nga > BALB/c > C57BL/6. In conclusion, neuronal IL-31RA expression in the DRG was the most important genetic factor affecting the severity of LLS and dermatitis in mice. Full article
(This article belongs to the Special Issue OSM/OSMR and Interleukin 6 Family Cytokines in Physiological and Pathological Condition 2.0)
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9 pages, 1789 KiB  
Article
Oncostatin M Counteracts the Fibrotic Effects of TGF-β1 and IL-4 on Nasal-Polyp-Derived Fibroblasts: A Control of Fibrosis in Chronic Rhinosinusitis with Nasal Polyps?
by Florent Carsuzaa, Émilie Béquignon, Matthieu Bainaud, Jean-François Jégou, Xavier Dufour, Jean-Claude Lecron and Laure Favot
Int. J. Mol. Sci. 2022, 23(11), 6308; https://doi.org/10.3390/ijms23116308 - 04 Jun 2022
Cited by 9 | Viewed by 1969
Abstract
Chronic rhinosinusitis with nasal polyps (CRSwNP) is associated with inflammation and tissue remodeling including myofibroblasts differentiation and extracellular matrix (ECM) deposition mediated by TGF-β1 and IL-4. Oncostatin M (OSM) is a cytokine involved in fibrotic processes in other cellular subtypes. We investigated the [...] Read more.
Chronic rhinosinusitis with nasal polyps (CRSwNP) is associated with inflammation and tissue remodeling including myofibroblasts differentiation and extracellular matrix (ECM) deposition mediated by TGF-β1 and IL-4. Oncostatin M (OSM) is a cytokine involved in fibrotic processes in other cellular subtypes. We investigated the mechanisms of action of OSM in the fibrosis process associated with CRSwNP. The expression of IL-4, OSM and TGF-β1 was assessed by RT-qPCR. Primary human cultures of nasal-polyp-derived fibroblasts were established and stimulated by TGF-β1 and/or IL-4 and/or OSM. The expression of ECM components and αSMA was determined by RT-qPCR and Western blot. TGF-β1-Smad3 signaling was investigated by immunofluorescence. TGF-β1, IL-4 and OSM as well as αSMA were overexpressed in nasal polyps when compared to noninflammatory nasal mucosa. In TGF-β1-stimulated nasal-polyp-derived fibroblasts, ECM genes and αSMA gene and protein were overexpressed, as well as αSMA in IL-4-stimulated fibroblasts. OSM counteracted the profibrotic effect of TGF-β1 on ECM components and αSMA. TGF-β1-induced nuclear translocation of Smad3 was completely reversed by OSM. OSM counteracts the profibrotic effect of IL-4 and also TGF-β1, by inhibiting the nuclear translocation of Smad3. We suggest OSM could be an efficient tool to protect against fibrosis in CRSwNP. Full article
(This article belongs to the Special Issue OSM/OSMR and Interleukin 6 Family Cytokines in Physiological and Pathological Condition 2.0)
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