فهرست نشریات علمی دسترسی آزاد ایران

Objective(s): Asthma is a heterogeneous disease. Neutrophilic asthma is associated with severe asthma and poor response to inhaled corticosteroids. We investigated whether 1,25-dihydroxyvitamin D3 can ameliorate neutrophilic airway inflammation, inhibit endoplasmic reticulum stress, and ERS-induced NLRP3 inflammasome activation in a murine model of neutrophilic asthma. Materials and Methods: BALB/c mice were established as an experimental model of neutrophilic asthma. 1,25-(OH)2D3 was administered for intervention to investigate the effect of Vitamin D3 on neutrophilic airway inflammation, ERS-induced NLRP3 activation. Inflammatory cells were counted in BALF, and lung tissue was histologically examined. Concentrations of IL-17, IL-1β, and IL-18 in BALF were measured. Immunohistochemical analysis of lung Ly-6G expression and AHR was tested. Furthermore, the percentage of Th17 cells was determined by flow cytometry. CHOP, GRP78, and NLRP3 protein expression was also examined by western blot. Results: We observed that the infiltration of inflammatory cells and goblet cell hyperplasia in lung and airway tissue were reduced by 1,25-(OH)2D3 treatment. The total number of inflammatory cells and the percentage of neutrophils in BALF were significantly less in the treatment groups. 1,25-(OH)2D3 obviously suppressed neutrophils infiltration and Ly-6G expression in neutrophilic asthma. 1,25-(OH)2D3 reduced Th17 cell percentage and IL-17 levels. The expression levels of GRP78 and CHOP were lower in the 1,25-(OH)2D3 treatment group than those in the NA model group. And, 1,25-(OH)2D3 decreased NLRP3 protein expression levels in the lungs of NA mice.Conclusion: Our results suggest that 1,25-dihydroxyvitamin D3 ameliorates neutrophilic asthma in mice by a mechanism linked to reduced ERS and NLRP3 inflammasome activation, supporting further investigation of its potential as a therapeutic candidate.