Abstract
We have shown that M. tuberculosis Cpn60.1 inhibits allergic lung inflammation and bronchial hyperresponsiveness in mice (Riffo-Vasquez Y et al. Clin Exp All. 2004). Here we have evaluated the effect of lower concentrations of Cpn60.1 on lung eosinophilia and leukocyte/endothelial cell interaction in vivo. Balbl/c mice were immunized twice with ovalbumin (ova, 10mg/mouse i.p. in alum). From day 14 all mice were exposed to ova (3%) once daily for 3 days and Cpn 60.1 was given i.n.15 min earlier. Lung lavages were performed 24 h after the last exposure. To examine the recruitment of cells in the microvasculature of the cremaster muscle, Cpn60.1 at 1μg/mouse was given s.c. into the scrotal sac of ova-sensitized mice followed by 100ng of eotaxin 10 minutes later. Four hours later the animals were prepared for intravital microscopy. Cpn60.1 at 0.001-1 μg/mouse inhibited the migration of eosinophils into the airways (ova 44.3±8.6 vs ova/60.1: 12.7±1.42; 13.3±3.4; 13.4±4.3 and 9.4±2.2×104/ml, n=10 for 0.001-1 μg of Cpn60.1 respectively, p≤ 0.05). Four hours after eotaxin injection, saline treated mice showed a significant accumulation of cells in the extra vascular tissue (saline: 40±5 vs Cpn60.1: 2.3±1 cells/50μm2, n=6) and higher number of cells rolling along the vessel wall in 30 sec (saline: 12±1.12 vs Cpn60.1: 2.8±1.02) compared to Cpn60.1 treated mice. In contrast, the adherence of cells to the endothelial layer was higher in Cpn60.1 compared to saline treated mice (saline adhesion: 15±1.7 vs Cpn60.1: 22.2±4.8 cells/50μm, n=6). Cn60.1 inhibits leukocyte migration to the lung in response to ova and prevented leukocyte rolling along and transmigration across the vessel wall in vivo.
- © 2011 ERS
