Baseline airway hyperreactivity in A/J mice is not mediated by cells of the adaptive immune system

Human asthma is characterized by increased airway hyperreactivity to a vari ety of bronchoconstricting agents. Aberrant type 2 immune responses in the lung have been associated with airway hyperreactivity in both human asthma and in murine models of allergic airways disease. Despite their intrinsical ly elevated basal airway reactivity to smooth muscle constricting agents, A /J mice demonstrated no inherent inflammatory cell infiltration nor elevati on of type 2 cytokines in the lung. Crossed bone marrow reconstitution expe riments between A/J and MHC congenic B10.A mice revealed enhanced airway re activity only in A/J recipients, irrespective of whether they had been reco nstituted with A/J or B10.A hemopoietic cells. Further, A/J-derived bone ma rrow cells did not affect the reactivity of B10.A recipients. Although mice on RAG-deficient and IL-4-deficient backgrounds demonstrate substantial ab rogation of allergen-induced airway hyperreactivity, these gene deletions h ad no impact on the elevated baseline reactivity when backcrossed onto A/J mice. Thus, in these mice, basal airway hyperreactivity is maintained indep endently of type 2 immunity induced by allergens.