In this latter study, the peribronchial NVP-BKM120 PI3K inhibitor attenuation value extracted from micro-CT images was significantly increased in sensitized mice as compared to control mice and was correlated with some remodeling components such as bronchial smooth muscle size. However, both inflammation and remodeling were present in this model and could account for the increased peribronchial attenuation. Moreover, inflammation spread over the boundaries of the bronchial wall within the lung parenchyma and could alter total lung attenuation. We thus hypothesized that the normalization of the peribronchial attenuation by the total lung attenuation could be more specific to assess bronchial remodeling. The aims of our study were then to develop a flexible mouse model of allergic asthma exhibiting inflammation alone, remodeling alone, or both characteristics together, to validate a semiautomatic method enabling a quick and reproducible assessment of peribronchial attenuation and total lung attenuation from micro-CT datasets, and to determine whether the peribronchial attenuation or the normalized peribronchial attenuation could be related to airway remodeling. Taken together, these results demonstrate that, using a flexible model of murine asthma, normalized PBA extracted from microCT examinations in living mice, can predict the presence of airway remodeling. The peribronchial attenuation value normalized by the total lung attenuation value was increased in mice exhibiting remodeling, was unchanged in mice exhibiting inflammation only, and was the best micro-CT parameter correlated with remodeling markers. In this study, we paid a special attention to build flexible challenge protocols based upon different endpoints which reproduced 3 features of human asthma, although the latter remains theoretical, since inflammatory cells are still present in fixed airways obstruction. Particularly, eosinophilic inflammation was observed in groups A and B only, while the main markers of remodeling, i.e. increased bronchial smooth muscle size and peribronchial fibrosis, were observed in groups B and C only. The use of Penh to assess BHR in mice deserves a specific comment. Indeed, Penh does not represent the airway resistance per se and it may vary according to the respiratory rate and/or experimental conditions. For instance, Penh is not accurate in C57BL6 mice. However, in our study, both Penh and LR ratios were similarly increased in OVA-sensitized mice as compared to control mice, which is in agreement with earlier studies performed in Balb/C mice. Moreover, invasive plethysmography cannot be performed longitudinally. BHR is one of the characteristics of asthma but the exact contribution of inflammation or remodeling remains undetermined. In our study, BHR assessed by the Penh ratio was only observed in mice exhibiting inflammation either alone or with remodeling. In small animals, even if clear model-dependent differences have been shown, Penh ratio has been shown to be mainly related to eosinophilic inflammation in Balb/C mice, which is consistent with our results. So far, to the best of our knowledge, there was no reported in vivo method able to assess bronchial remodeling noninvasively. By contrast, airway inflammation can be assessed through exhaled nitric oxide or induced sputum. In the present study, we demonstrated that micro-CT can quantify remodeling noninvasively in sensitized mice. However, PBA and normalized PBA were also correlated with some parameters of bronchial inflammation. These results can be partly explained by the close relationship between inflammation and remodeling, which is likely to entail potential cross-correlations. Our 3 endpoints protocol allowed us to demonstrate the absence of any significant difference in micro-CT parameters between sensitized and control mice from group A.