NITRIC-OXIDE PATHWAY IS INDUCED BY FC-EPSILON-RI AND UP-REGULATED BY STEM-CELL FACTOR IN MOUSE MAST-CELLS

Murine stem cell factor (SCF) induces the differentiation of mucosal m ast cells (MMC) into connective tissue mast cells (CTMC) and potentiat es mediator release induced by aggregation of high-affinity IgE recept ors (Fc epsilon RI). In the present work, we investigated the effect o f Fc epsilon RI aggregation on nitric oxide (NO) pathway induction in the different subsets of mast cells, as well as the contribution of SC F in this induction. Inducible NO synthase (iNOs) expression was not e videnced in non-stimulated MMC obtained by culture of hematopoietic pr ogenitors in the presence of interleukin-3, whereas IgE-antigen-stimul ated MMC expressed iNOs mRNA and protein and synthesized nitrites. Lon g-term treatment of MMC with SCF, allowing them to differentiate into CTMC, induced iNOs expression in non-stimulated cells and up-regulated iNOs expression and generation of NO derivatives induced by IgE-antig en stimulation. Thus, NO derivatives generated by mast cells could par ticipate in inflammatory reactions during allergic stimulation.