Creating an animal model of pulmonary emphysema, a type of COPD, requires exposure to cigarette smoke (CS) for more than 3 months. The pulmonary emphysema model was induced by combination of CS exposure and polyinosinic-polycytidylic acid [poly(I:C)] administration for 4 weeks in mice, and the effects of anti-thymic stromal lymphopoietin (TSLP) antibody (Ab) and rolipram (Rol) were examined.
CS was exposed for 4 weeks (Days 1 to 26) and poly(I:C) was administered nasally for 4 days. From Days 15 to 25, the anti-TSLP Ab was nasally administered every other day, and Rol was orally administered daily. In the model, the peak expiratory flow (PEF) and forced expired volume at 0.05 sec/forced expired volume (FEV_0.05/FVC) were decreased, and the tissue damping, inflammatory cells in bronchoalveolar lavage fluid (BALF) and lung tissue, and pulmonary air space size were increased on Day 27. The anti-TSLP Ab inhibited the decrease in PEF and the increase in eosinophils in BALF, but Rol did not suppress these changes.
Based on these results, in the pulmonary emphysema model, respiratory function depression, inflammatory cells infiltration and alveolar expansion were observed, and the anti-TSLP Ab inhibited the respiratory function depression and inflammatory cells infiltration, but the effect of Rol was not clear.