Figure 1. GCs inhibit lung inflammation by the GR in myeloid cells requiring an intact GR dimerization interface.

(a) GR^flox and GR^LysMCre mice were injected with vehicle (Co), LPS and OA (hereafter, the LPS and OA co-treatment will be designated as ‘LPS') or LPS and Dex (LPS+Dex). After 18 h, EB was injected i.v., and the mice were killed 30 min later. EB accumulation in the lung was determined after perfusion with PBS+5 mM EDTA. (b) Representative haematoxylin/eosin (H&E) staining of lung sections (scale bars, 0.1 mm), and (c) histological scores of GR^flox and GR^LysMCre mice treated as described in a. (d) GR^flox and GR^LysMCre mice were treated as described in a. Cell numbers were determined in the BAL 18 h after the indicated treatments. (e) GR^dim and wild-type (WT) littermate mice were injected with vehicle (Co), LPS or LPS+Dex. After 24 h, EB was injected i.v. and 30 min later the mice were killed. EB accumulation in the lung was quantified as described in a. (f) Representative H&E staining of lung sections (scale bars, 0.1 mm) and (g) histological scores of lungs of littermate WT and GR^dim mice from the experiment described in e. (h) GR^dim and WT mice were treated as described in e. Cell numbers were determined in the BAL 24 h after the indicated treatments. Results are presented as mean±s.e.m. Number of biological replicates: (a) (6–10), (c) (18–20), (d) (7–13), (e) (4–8), (g) (12–16) and (h) (7–11). In a, data are from three independent biological experiments; in c, data are from four independent biological experiments; in d, data are from two independent biological experiments; in e, data are from two independent biological experiments; in g, data are from three independent biological experiments out of four; and in h, data are from two independent biological experiments. Statistical analysis was performed by one-way analysis of variance. *P<0.05, **P<0.01, ***P<0.001; ND, not detectable; NS, not significant.