Abstract

Objective To verify the hypothesis that NLRP3-dependent IL-1β and IL-18 play a pathogenic role in mice with asthma.Methods A total of 21 C57BL/6 mice were randomly divided into 3 groups:the control group,NLRP3 inhibitor glyburine group and asthma group (n =7).A mouse model of allergic asthma was established by sensitization and challenge with ovalbumin for the mice in glyburine group and asthma group.Glyburine at 0.5 mg/g was given to the mice in glyburine group by intraperitoneal injection 30 minutes before inhaling ovalbumin.After induction of asthma,the airway responsiveness was measured and the pathological change in lung tissues was observed with HE r=0.856,P=0.014).Conclusion High expressions of NLRP3,IL-1β and IL-18 in the lungs of mice with asthma could be inhibited with glyburine treatment,suggesting NLRP3-dependent IL-1β and IL-18 play a crucial role in the development of allergic airway disease. Key words: NLRP3; IL-1β; IL-18; Allergic airway disease

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