The following is a summary of “Evidence that oncostatin M synergizes with IL-4 signaling to induce TSLP expression in chronic rhinosinusitis with nasal polyps,” published in the MAY 2023 issue of Allergy & Immunology by Wang, et al.

For a study, researchers sought to investigate the impact of oncostatin M (OSM) on the synthesis and release of thymic stromal lymphopoietin (TSLP) from nasal epithelial cells (NECs) in patients with chronic rhinosinusitis with nasal polyps (CRSwNP) and its association with type 2 inflammation.

Mucosal tissue and primary NECs were collected from patients with CRSwNP. The expression of OSM receptors, IL-4 receptors (IL-4R), and TSLP was assessed using quantitative PCR and immunofluorescence. Air-liquid interface-cultured NECs were stimulated with cytokines, including OSM, and various techniques such as quantitative PCR, ELISA, Western blot, and flow cytometry were used to evaluate the expression of OSM receptors, IL-4 receptors (IL-4R), and TSLP.

Nasal polyp tissues and NECs from patients with CRSwNP exhibited elevated levels of OSM receptor β chain (OSMRβ), IL-4Rα, and TSLP compared to control tissues and cells. The expression of OSMRβ in tissue was positively correlated with the levels of IL-4Rα and TSLP. Stimulation of NECs with OSM increased the expression of OSMRβ and IL-4Rα. Furthermore, stimulation with both IL-4 and OSM synergistically enhanced the production of TSLP, which was inhibited by a signal transducer and activator of transcription 6 inhibitor. The combination of IL-4 and OSM also upregulated the expression of proprotein convertase subtilisin/kexin 3, an enzyme involved in the processing and activation of TSLP.

OSM promotes type 2 inflammation in CRSwNP by increasing the expression of IL-4Rα and collaborating with IL-4 to induce the synthesis and release of TSLP from NECs. The results suggested that OSM not only triggers TSLP synthesis but also facilitates its posttranslational processing and activation through proprotein convertase subtilisin/kexin 3, thereby contributing to type 2 inflammation in CRSwNP.

Source: jacionline.org/article/S0091-6749(23)00003-9/fulltext