Mast cells can revert dexamethasone-mediated down-regulation of stem cell factor

Mast cell hyperplasia can be causally related with chronic inflammation and liver fibrosis. Their survival and proliferation is dependent upon locally produced growth factors, the major one being the stem cell factor (SCF). G lucocorticoids can decrease mastocytosis, down-regulating the mast cell pro duction of pro-inflammatory factors or inhibiting the expression of SCF in stroma. We compared dexamethasone effect on SCF expression in co-cultures o f mast cells with NIH/3T3 fibroblasts or with primary cultures of activated hepatic stellate cells. Dexamethasone abrogated the NIH/3T3 stroma capacit y to sustain mast cell proliferation, but not of hepatic stellate cells, at the post-transcriptional level. Mast cells reverted completely dexamethaso ne effect on hepatic stellate cells, increasing their SCF synthesis and tra nsport. In both models, dexamethasone inhibited the mast cell spreading on the stroma, which was thus not required for mast cell survival and prolifer ation. Liver pathologies associated with mast cell hyperplasia are not expe cted to be sensitive to glucocorticoid treatments. (C) 2001 Published by El sevier Science B.V.