Oxidative stress is well known to be implicated in the development of asthma. The mitochondrial respiratory chain is a major site of intracellular reactive oxygen species (ROS) generation and, at the same time, an important target for the damaging effects of ROS. Mito-Tempo is a specific mitochondrial ROS inhibitor and it is known to be associated with opening of mi-tochondrial permeability transition pore and inhibition of cell necroptosis or apoptosis. However, there is little information on the protective effects of Mito-Tempo on the inflammatory airway disorders including bronchial asthma and its acute exacerbation. We investigate the effects of Mito-tempo on the allergic airway inflammation and hyperresponsiveness using the mice sensitized with OVA and LPS and then challenged with OVA (OVALPS-OVA mice). The OVALPS-OVA mice showed the typical features of neutrophilic asthma; increased airway inflammatory cells, the pathologic changes, the increased levels of Th2 cytokines in lungs of OVALPS-OVA mice, increased mitochondrial ROS generation, and increased bronchial hyperresponsiveness. Interestingly, we found that in OVALPS-OVA mice, Mito-Tempo, a novel mitochondrial targeting agent significantly reduced the increases in inflammatory cytokines, mitochondrial ROS generation, airway inflammation, and bron-chial hyperresponsiveness. These findings indicate that mitochondrial dysfunction including oxidative damage may be im-plicated in the pathogenesis of bronchial asthma and provide the therapeutic potential of a mitochondrial targeting agent, Mito-Tempo, for bronchial asthma.