Premium
Changes in light‐scatter profile, membrane depolarization and calcium mobilization of neutrophils induced by G‐CSF in vivo
Author(s) -
Spiekermann Karsten,
Emmendoerffer Andreas,
Elsner Jörn,
Raeder Evelin,
LohmannMatthes M.L.,
Welte Karl,
Roesler Joachim
Publication year - 1994
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1994.tb05066.x
Subject(s) - depolarization , stimulation , neutropenia , in vivo , ionomycin , calcium , endocrinology , medicine , granulocyte , chemistry , immunology , biology , chemotherapy , microbiology and biotechnology
Summary. To extend our studies about phenotypical and functional alterations of G‐CSF‐induced neutrophils we have evaluated their light‐scatter profile, mobilization of intracellular calcium ([Ca 2+ ]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 injection in the latter group. We found an impairment of [Ca 2+ ]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, [Ca 2+ ]i fluxes were normal when ionomycin was used. Neutrophils from patients with cyclic neutropenia (cyNP) and chemotherapy‐induced neutropenia (chNP) mobilized [Ca 2+ ]i similar to those from healthy donors. Furthermore, we found a decreased percentage of neutrophils depolarizing after stimulation with fMLP and PMA in patients with SCN, whereas membrane depolarization was normal in patients with chNP and cyNP. All the alterations found here are suggested to be caused by a partial immaturity of the neutrophils, although in vivo activation and a direct effect of G‐CSF on myeloid precursors might be involved.