Eur J Pediatr (2011) 170:1495–1505 Fig. 1 Genomic and nongenomic action of glucocorticoids. GC, glucocorticoid; cGR, cytoplasmic GC receptor; mGR, membrane- bound GC receptor; HSP90, heat shock protein 90; Src, protein. For explanation, please see the text. (Adapted by Buttgereit et al. [10] and Stahn et al. [70]) 1497 production of arachidonic acid and mediators of lipoox- ygenase and cyclooxygenase pathway as well as of PAF [57]. It is assumed that the activation of the cell by a noxious stimulus causes the inactivation of lipocortines and development of inflammation. On the contrary, the in- creased production of lipocortines induced by GCs has opposite, anti-inflammatory effects [57]. GCs reduce the penetration of neutrophils into the lungs, decreasing their adherence to the endothelium and thereby increasing secondarily a count of circulating neutrophils [30, 50, 51, 55, 66]. Moreover, GCs decrease the counts of circulating mononuclears, eosinophils and basophils as well as the synthesis of cytokines by macrophages, eosinophils and T lymphocytes. GCs stabilize lysosomes, inhibit the release of lysosomal enzymes, chemotaxia and other functions of neutrophils as well [34]. Furthermore, GCs stimulate the production of secretion leukocyte protease inhibitor, an important antiprotease, which may suppress an inflammation in the airways. GCs facilitate the transcription of β2-receptor gene and reduce the mast cells count and production of mucus in the airways, too. By stabilizing the cell membranes and decreasing the production of pro- inflammatory and vasoactive substances, GCs reduce micro- vascular permeability. In addition, by direct modulation of the pulmonary vasomotoric tone, GCs diminish pulmonary vasoconstriction and inhibit fibrogenesis [24, 34]. Fig. 2 Trans-activation or trans- repression of gene caused by GC–GR binding in cell nucleus. GC, glucocorticoid; cGR, cyto- + plasmic GC receptor; GRE , positive glucocorticoid respon- sive element; GRE−, negative glucocorticoid responsive ele- ment; IL, interleukin; AP-1, protein activator-1; NFκB, nu- clear factor κB; IRF3, interferon regulatory factor 3. For expla- nation, please see the text