Figure 1.

The chronic inflammatory pathologies occurring in I5/hE2 mice are completely dependent on one or more eosinophil effector functions. Representative airways from coronal lung sections from wild-type (C57BL/6J) mice are shown in comparison to airways in similar sections from age-matched (12 wk postpartum) double-transgenic (I5/hE2) mice and triple-transgenic (eosinophilless transgenic animals, PHIL/I5/hE2). Sections stained with hematoxylin-eosin (H&E) and periodic acid-Schiff (PAS) provide evidence of the eosinophil-dependent pulmonary changes (inflammatory cell infiltrate and lung structural perturbations [H&E] and goblet cell metaplasia/epithelial cell mucin accumulation [PAS], respectively) that occurred in the parental I5/hE2 model and lost in the absence of eosinophils, but not cytokine/chemokine transgene expression (PHIL/I5/hE2). Scale bar, 50 μm