Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Oncostatin M’s Involvement in the Pathogenesis of Chronic Rhinosinusitis: Focus on Type 1 and 2 Inflammation

Version 1 : Received: 16 October 2023 / Approved: 16 October 2023 / Online: 17 October 2023 (08:05:36 CEST)

A peer-reviewed article of this Preprint also exists.

Ishikawa, C.; Takeno, S.; Okamoto, Y.; Kawasumi, T.; Kakimoto, T.; Takemoto, K.; Nishida, M.; Ishino, T.; Hamamoto, T.; Ueda, T.; Tanaka, A. Oncostatin M’s Involvement in the Pathogenesis of Chronic Rhinosinusitis: Focus on Type 1 and 2 Inflammation. Biomedicines 2023, 11, 3224. Ishikawa, C.; Takeno, S.; Okamoto, Y.; Kawasumi, T.; Kakimoto, T.; Takemoto, K.; Nishida, M.; Ishino, T.; Hamamoto, T.; Ueda, T.; Tanaka, A. Oncostatin M’s Involvement in the Pathogenesis of Chronic Rhinosinusitis: Focus on Type 1 and 2 Inflammation. Biomedicines 2023, 11, 3224.

Abstract

ABSTRACT: Objectives: Oncostatin M (OSM), a member of the interleukin (IL)-6 family of cytokines, is known to elicit pathogenic effects involving disruption of the epithelial barrier function as a part of immunological response networks. It is not yet known how these integrated cytokine signals influence inflammation and other physiological processes in the pathology of chronic rhinosinusitis (CRS). We investigated the expression and distribution of OSM and OSM receptor (OSMR) in sinonasal specimens of CRS patients, and we compared the results with a panel of inflammatory cytokine levels and clinical features. Materials and Methods: We classified CRS patients as eosinophilic (ECRS, n=36) or non-eosinophilic (non-ECRS, n=35) based on the Japanese Epidemiological Survey of Refractory Eosinophilic Chronic Rhinosinusitis (JESREC) phenotypic criteria, and we compared their cases with those of 68 non-CRS subjects. We also examined stimulatory effects of OSM on the expression levels of cytokine receptors by using the human bronchial epithelium cell line BEAS-2B. Results: An RT-PCR showed that the OSM mRNA levels were significantly increased in the ethmoid sinus mucosa of the CRS patients. The OSM mRNA levels were positively correlated with those of TNF-α, IL-1β, IL-13, and OSMR-β. In BEAS-2B cells, OSM treatment induced significant increases in the OSMR-β, IL-1R1, and IL-13Ra mRNA levels. Conclusions: Our findings indicate that OSM is involved in the pathogenesis of CRS in both type 1 and type 2 inflammation, suggesting the OSM signaling pathway as a potential therapeutic target for modulating epithelial stromal interactions.

Keywords

paranasal sinus; chronic rhinosinusitis; CRS; epithelial cell; eosinophil; oncostatin M; OSM; OSM receptor; OSMR

Subject

Medicine and Pharmacology, Otolaryngology

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