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Coordinated regulation of eosinophil production and migration by glucocorticoids, prostaglandins, and cysteinyl-leukotrienes.

Int Immunopharmacol

January 2025

Laboratório de Citocinas Dept. of Immunology Instituto de Microbiologia Prof. Paulo de Góes Universidade Federal do Rio de Janeiro Rio de Janeiro Brazil.

Introduction: The spectrum of eosinophil functions has expanded from fighting helminths to multiple novel roles in malignancy, infection, cancer, and metabolism. In asthma, glucocorticoids, prostaglandins (PG), and cysteinyl-leukotrienes (LT) regulate eosinophil biology through separate signaling pathways. Here we've evaluated the complex interplay between Dexa, PGE2, and CysLTs in eosinopoiesis and eosinophil biology in an allergic asthma model.

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Objective: This study seeks to elucidate the role and molecular mechanisms of IL-8 in nasal epithelial cell pyroptosis and its impact on glucocorticoid (GC) resistance.

Methods: We assessed the expression of pyroptosis-related biomarkers and IL-8 in tissues and human nasal epithelial cells (hNECs) from both control and nasal polyp patients using western blot. Their localization was determined through immunohistochemistry and immunofluorescence.

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The clinical use of dexamethasone (DXM) is associated with the development of non-alcoholic fatty liver disease (NAFLD). However, the mechanisms by which DXM-induced NAFLD is still incompletely known. Therefore, the current study aims to test the hypothesis that DXM-induced NAFLD is mediated by dysregulation of key genes involved in lipid metabolism and liraglutide (LG) can ameliorate these effects.

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Objectives: To explore the mechanism by which histone deacetylase 1 (HDAC1) regulates steroid-induced apoptosis of mouse osteocyte-like MLO-Y4 cells.

Methods: MLY-O4 cells were treated with 400 nmol/L trichostatin A (TSA) or 1 mmol/L dexamethasone for 24 h or transfected with a HDAC1-overexpressing vector prior to TSA or dexamethasone treatment. The changes in the expressions of HDAC1, SP1, cleaved caspase-3 and Bax, SP1 acetylation level, cell proliferation, and cell apoptosis were examined.

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Cushing's syndrome is a rare disease caused due to prolonged exposure to excess glucocorticoids. Although rare, diagnosing Cushing's syndrome is clinically significant as it allows tailored and timely management and significant reduction or even prevention of the comorbidities caused by cortisol excess. This report delineates the presentation of a 44-year-old female with refractory secondary hypertension and severe hypokalaemia, initially thought to be caused by hyperaldosteronism.

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