Spiekermann, K.K.SpiekermannEmmendörffer, A.A.EmmendörfferElsner, J.J.ElsnerRaeder, E.E.RaederLohmann-Matthes, M.-L.M.-L.Lohmann-MatthesRoesler, J.J.RoeslerWelte, K.K.Welte2022-03-032022-03-031994https://publica.fraunhofer.de/handle/publica/18429910.1111/j.1365-2141.1994.tb05066.xTo extend our studies about phenotypical and functional alterations of G-CSF-induced neutrophils we have evaluated their light-scatter profile, mobilization of intracellular calcium ([Ca2+]i) and membrane depolarization after stimulation. A significant increase in the forward scatter signals could be demonstrated in such neutrophils from patients with neutropenias of various origin and from healthy test subjects. This increase began 4 h and returned to normal 96 h after G-CSF injections in the latter group. We found an impairment of [Ca2+]i mobilization in neutrophils from patients with glycogen storage disease type IB after stimulation of these cells with fMLP. It was even more pronounced than in severe congenital neutropenia (SCN). However, [CA2+]i fluxes were normal when ionomycin was used. Neutrophils from patients with cyclic neutropenia (cyNP) and chemotherapy-induced neutropenia (chNP) mobilized [CA2+]i similar to those from healthy donors. (abstract truncated)engranulocytesimmunologyneutropenianeutrophilssignal transduction615610620616journal article