Research Paper Volume 10, Issue 6 pp 1415—1423

Induction of neutrophil apoptosis by a Bcl-2 inhibitor reduces particulate matter-induced lung inflammation

Figure 3. Delayed resolution of PM-induced lung inflammation in vav-Bcl-2 transgenic mice. To further examine the role of Bcl-2 in regulation of lung inflammation in vivo, vav-Bcl-2 transgenic mice (Bcl-2 overexpressing mice) were instilled with PM at 100 μg/d/mouse for 2 days (n=5 to 7 per group). This resulted in marked accumulation of total inflammatory cells and neutrophils in the bronchoalveolar lavage fluid (BALF). Both of these were significantly increased in the vav-Bcl-2 transgenic mice (A-C) after 24 h, 48 h, and 96 h instillation of PM. Histochemical staining (HE) identified inflammatory cell recruitment (scale bar=100 μm). Elevated levels of inflammatory cells were recruited in bcl-2 overexpressed mice. There was delayed resolution of inflammation in bcl-2 overexpressing mice (D and E). The expression of CXCL-1 and CXCL-2 were also analyzed at 24, 48 and 96 h after instillation with PM solution (E).