How little is known about genetic differences between the commercially available inbred mouse strains, which makes it hard to link phenotypic differences in parameters to genetic variability. So far, our ventilatory, inflammatory and immunologic results can only be linked to a predominant Th1- or Th2-bias. Clear differences were found in airway hyper-reactivity to methacholine in the different mouse strains. Th2-biased mouse strains showed increases in airway hyper-reactivity compared to Th1-biased mice, as already shown by different other research groups in other asthma models. However, one exception is the AKR strain, which although being Th1-biased, responded significantly in terms of increase in airway hyper-reactivity. Furthermore, we found differences in baseline reactivity to methacholine between the different Th2-biased mice. BP2 and A/J mice were found to be more Niraparib sensitive to methacholine provocation than BALB/c mice and this both for the TDI-treated animals and the control mice. Among the three Th2-biased strains, the BALB/c mice presented the best separation between TDI-sensitized plus TDI-challenged animals and the controls. Differences in baseline airway hyper-reactivity can be an intrinsic characteristic of the mouse strain. Differences in alveolar size, lung volume, elastic properties and differences in controlling smooth muscle cells by the autonomic nerve system have been described. When we analyse our results of the airway hyper-reactivity more in detail, we can conclude that individual adjustments for methacholine concentrations per mouse strain are preferable. A/ J mice reach a plateau at 10 mg/ml methacholine, while C57Bl/6 mice are still at a submaximum at that concentration. We chose to perform the methacholine provocation with the same methacholine concentrations for each mouse strain to make comparisons easier. In our model, airway inflammation in TDI-induced asthma is characterized by an influx of mainly neutrophils and also some eosinophils. This study showed that BALB/c mice have the most pronounced airway inflammation of all 7 mouse strains. However, our observations support that there is no consistent relationship between airway hyper-reactivity and the influx of neutrophils and eosinophils in the lungs, as already shown by Whitehead et al. When using ovalbumin models, C57Bl/6 are often used and they respond with a robust airway eosinophilic response. It is conceivable, as suggested by Herrick et al., that the ability to generate airway inflammation after chemical exposure is under different and perhaps tighter genetic control than the ability to mount these responses after exposure to other antigens. Significant increases in the total amount of Th-, Treg-, Tc- and B-lymphocytes were found in all Th2-biased mouse strains and for some lymphocyte subpopulations also for the Th1-biased CBA and AKR mice. Vogelsang et al. already showed that there are different amounts of conventional and plasmacytoid dendritic cells and Treg-lymphocytes in blood and spleen of BALB/c vs. C57Bl/ 10J mice.