Figure 6.

The chronic pulmonary pathologies displayed by I5/hE2 mice do not occur as a function of leukotriene-mediated events. Representative airways in coronal lung sections from C57BL/6J mice wild-type (negative controls) and age-matched (12 wk postpartum) double-transgenic I5/hE2 mice (positive controls) are shown in comparison to airways in similar sections from transgenic mice targeting all leukotrienes (5-LO^−/−/I5/hE2), the LTB₄ high-affinity receptor (BLT-1^−/−/I5/hE2), or I5/hE2 mice treated with the cys-leukotriene antagonist drug, montelukast (MK/I5/hE2). Sections were stained with H&E and PAS. These data provide evidence of increased inflammatory cell infiltrates, lung structural perturbations (H&E), and goblet cell metaplasia/epithelial cell mucin accumulation (PAS), all of which remained unchanged in the cohorts of double-transgenic mice, despite the targeting of leukotriene pathways activities. Scale bars, 100 μm. B, bronchiole; PV, pulmonary vessel.