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We established a selection strategy to identify new models for an altered airway inflammatory response from a large compendium of mutant mouse lines that were systemically phenotyped in the German Mouse Clinic (GMC). As selection criteria we included published gene functional data, as well as immunological and transcriptome data from GMC phenotyping screens under standard conditions. Applying these criteria we identified a few from several hundred mutant mouse lines and further characterized the  Cox4i2 tm1Hutt  ,  Ifit2 tm1.1Ebsb  , and  Prdm11 tm1.1ahl   lines following ovalbumin (OVA) sensitization and repeated OVA airway challenge. Challenged  Prdm11 tm1.1ahl   mice exhibited changes in B cell counts, CD4 +  T cell counts, and in the number of neutrophils in bronchoalveolar lavages, whereas challenged  Ifit2 tm1.1Ebsb   mice displayed alterations in plasma IgE, IgG1, IgG3, and IgM levels compared to the challenged wild type littermates. In contrast, challenged  Cox4i2 tm1Hutt   mutant mice did not show alterations in the humoral or cellular immune response compared to challenged wild type mice. Transcriptome analyses from lungs of the challenged mutant mouse lines showed extensive changes in gene expression in  Prdm11 tm1.1ahl   mice. Functional annotations of regulated genes of all three mutant mouse lines were primarily related to inflammation and airway smooth muscle (ASM) remodeling. We were thus able to define an effective selection strategy to identify new candidate genes for the predisposition to an altered airway inflammatory response under OVA challenge conditions. Similar selection strategies may be used for the analysis of additional genotype – envirotype interactions for other diseases.

plos one

Cox4i2, Ifit2, and Prdm11 Mutant Mice: Effective Selection of Genes Predisposing to an Altered Airway Inflammatory Response from a Large Compendium of Mutant Mouse Lines