The NLRP3 inflammasome is an intracellular complex that regulates release of proinflammatory cytokines such as IL-1β, in response to exogenous pathogen-associated molecular patterns and endogenous danger signals. Recently, various auto-in-flammatory or chronic inflammatory disorders have been introduced as an inflammasome related disorders. However, the role of inflammsome in allergic airway diseases is controversial. In this study, we have investigated the role of inflammasome in HDM-induced bronchial asthma and the interaction between mitochondrial ROS generation and NLRP3 inflammasome activation. HDM-sensitized and -challenged mice showed the typical allergic airway inflammatory features. Very interestingly, the administration of OTC restored the levels of GSH, decreased the levels of NLRP3 expression and IL-1β in lungs, the numbers of airway inflammatory cells in BAL fluids, the peribronchial and perivascular inflammation in lung tissues, the in-crease in the levels of inflammatory cytokines, and bronchial hyperresponsiveness in HDM-sensitized and -challenged mice. Moreover, OTC significantly reduced the mitochondrial ROS generation in lungs of HDM-induced asthma. Blockade of IL-1β using neutralizing antibody resulted in the substantial improvement of asthmatic features. These findings suggest that NLRP3 inflammasome plays a crucial role in the pathogenesis of HDM-induced asthma and its activation is closed related to oxidative stress, especially due to mitochondrial ROS production.