Chemerin and IL‐17 are potential predictors and Chemerin silencing alleviates inflammatory response and bone remodeling in chronic rhinosinusitis

Abstract

Chronic rhinosinusitis (CRS) is an inflammatory disease of paranasal sinuses. This study is formulated to explore the roles of pro‐inflammatory factors Chemerin and interleukin‐17 (IL‐17) in CRS. Patients suffering from CRS without/with nasal polyps (CRSsNP/CRSwNP), along with volunteers, were recruited. CRS rabbit models were constructed by Staphylococcus aureus infection and rabbits were injected with lentiviral vectors of short hairpin RNA‐targeting Chemerin (shChemerin), followed by micro‐computed tomography (CT) scan. Levels of Chemerin and IL‐17 were determined, and histopathological lesions were observed in subjects and CRS rabbits. Correlations between Chemerin/IL‐17 level and Lund‐Mackay/Lund‐Kennedy scores of subjects and the predictive value of Chemerin or IL‐17 for CRS were analyzed. In CRS patients and rabbits, inflammatory degrees and the level of Chemerin/IL‐17 were increased in pathological tissues or plasma, while Chemerin silencing alleviated CRS symptoms of CRS rabbits. Chemerin and IL‐17 were mainly located in the immune cells of pathological tissues and presented the positive correlation with Lund‐Mackay/Lund‐Kennedy score of CRS patients. Also, they showed high predictive value for CRS. Micro‐CT scan uncovered that CRS rabbits had increased bone remodeling, which was alleviated by Chemerin silencing. Collectively, Chemerin and IL‐17 are potential predictors and Chemerin silencing alleviates inflammatory response and bone remodeling in chronic rhinosinusitis.

Chemerin Levels in Individuals with Type 2 Diabetes and a Normal Weight versus Individuals with Type 2 Diabetes and Obesity: An Observational, Cross-Sectional Study

“…Chemerin is a critical player in metabolic and immune regulation, particularly in diseases which provoke systemic inflammatory conditions [8,[52][53][54]. The proteolytic cleavage and regulatory patterns of chemerin are consistent across human and mouse models, with several studies indicating that variation in inflammatory responses between conditions such as rheumatoid arthritis and osteoarthritis is linked to the generation of different chemerin forms by proteolysis [11,12].…”