{'fraction_non_alphanumeric': 0.02930728241563055, 'fraction_numerical': 0.0008880994671403197, 'mean_word_length': 5.748502994011976, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Nitric oxide pathway is induced by FcεRI and up‐regulated by stem cell factor in mouse mast cells

Murine stem cell factor (SCF) induces the differentiation of mucosal mast cells (MMC) into connective tissue mast cells (CTMC) and potentiates mediator release induced by aggregation of high‐affinity IgE receptors (FcεRI). In the present work, we investigated the effect of FcεRI aggregation on nitric oxide (NO) pathway induction in the different subsets of mast cells, as well as the contribution of SCF in this induction. Inducible NO synthase (iNOs) expression was not evidenced in non‐stimulated MMC obtained by culture of hematopoietic progenitors in the presence of interleukin‐3, whereas IgE‐antigen‐stimulated MMC expressed iNOs mRNA and protein and synthesized nitrites. Long‐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‐antigen stimulation. Thus, NO derivatives generated by mast cells could participate in inflammatory reactions during allergic stimulation.