Ca2+ ionophores inhibit superoxide generation by chemotactic peptide in rabbit neutrophils and the correlation with intracellular calcium

1988 ◽  
Vol 84 (1) ◽  
Author(s):  
Jose Jacob
Keyword(s):  
Intracellular Calcium ◽  
Chemotactic Peptide ◽  
Superoxide Generation

scholarly journals Regulation of superoxide generation by myeloperoxidase during the respiratory burst of human neutrophils

1986 ◽  
Vol 237 (2) ◽  
pp. 601-604 ◽  
Author(s):  
S W Edwards ◽  
T F Swan
Keyword(s):  
Respiratory Burst ◽  
Cytochalasin B ◽  
Superoxide Radical ◽  
Human Neutrophils ◽  
Second Phase ◽  
Chemotactic Peptide ◽  
O2 Uptake ◽  
Superoxide Generation ◽  
Lower Magnitude

The role of myeloperoxidase in the regulation of the respiratory burst of human neutrophils activated by the chemotactic peptide (N-formyl-L-methionyl-L-leucyl-L-phenylalanine) plus cytochalasin B was determined by using anti-(human myeloperoxidase) antibody. The respiratory burst activated under these conditions consisted of an initial (1-2 min) phase with high rates of O2 uptake, luminol-dependent chemiluminescence and superoxide radical (O2-.) generation and a second, more sustained, phase of lower magnitude of chemiluminescence and O2 uptake: O2-. generation did not occur during this second phase. In cell suspensions stimulated in the presence of anti-(human myeloperoxidase) antibody, the magnitude of the initial phase of both O2 uptake and O2-. generation was unaffected, but these high rates were maintained over much longer periods than in control suspensions. It is therefore proposed that a product of myeloperoxidase normally regulates the duration of O2-. generation during the respiratory burst, possibly by inhibition of NADPH oxidase.

scholarly journals Modulation of cytosolic-free calcium transients by changes in intracellular calcium-buffering capacity: correlation with exocytosis and O2-production in human neutrophils.

1984 ◽  
Vol 99 (4) ◽  
pp. 1212-1220 ◽  
Author(s):  
P D Lew ◽  
C B Wollheim ◽  
F A Waldvogel ◽  
T Pozzan
Keyword(s):  
Intracellular Calcium ◽  
Human Neutrophils ◽  
Free Calcium ◽  
Calcium Stores ◽  
Chemotactic Peptide ◽  
Functional Responses ◽  
Cytosolic Free Calcium ◽  
Calcium Buffering ◽  
O2 Production ◽  
Granule Release

The intracellularly trapped fluorescent calcium indicator, quin 2, was used not only to monitor changes in cytosolic-free calcium, [Ca2+]i, but also to assess the role of [Ca2+]i in neutrophil function. To increase cytosolic calcium buffering, human neutrophils were loaded with various quin 2 concentrations, and [Ca2+]i transients, granule content release as well as superoxide [O2-] production were measured in response to the chemotactic peptide formyl-methionyl-leucyl-phenylalanine (fMLP) and the calcium ionophore ionomycin. Receptor-mediated cell activation induced by fMLP caused a rapid rise in [Ca2+]i. The extent of [Ca2+]i rise and granule release were inversely correlated with the intracellular concentration of quin 2, [quin 2]i. These effects of [quin 2]i were more pronounced in the absence of extracellular Ca2+. The initial rate and extent of fMLP-induced O2- production were also inhibited by [quin 2]i. The rates of increase of [Ca2+]i and granule release elicited by ionomycin were also inversely correlated with [quin 2]i in Ca2+-containing medium. As the effects of ionomycin, in contrast to those of fMLP, are sustained, the final increase in [Ca2+]i and granule release were not affected by [quin 2]i. A further reduction of fMLP effects was seen when intracellular calcium stores were depleted by incubating the cells in Ca2+-free medium with ionomycin. The specificity of quin 2 effects on cellular calcium were confirmed by loading the cells with Anis/AM, a structural analog of quin 2 with low affinity for calcium which did not inhibit granule release. In addition, functional responses to phorbol myristate acetate (PMA), which stimulates neutrophils without raising [Ca2+]i, were not affected by [quin 2]i. The findings indicate that rises in [Ca2+]i control the rate and extent of granule exocytosis and O2-generation in human neutrophils exposed to the chemotactic peptide fMLP.

Dynamics of chemotactic peptide-induced superoxide generation by human monocytes

Inflammation ◽  
1987 ◽  
Vol 11 (2) ◽  
pp. 229-240 ◽  
Author(s):  
Edward J. Leonard ◽  
Amala Shenai ◽  
Alison Skeel
Keyword(s):  
Human Monocytes ◽  
Chemotactic Peptide ◽  
Superoxide Generation

Potentiation of Chemotactic Peptide-Induced Superoxide Generation by CD38 Ligation in Human Myeloid Cell Lines

1997 ◽  
Vol 121 (5) ◽  
pp. 949-956 ◽  
Author(s):  
N. Tsujimoto ◽  
K. Kontain ◽  
S.-i. Inoue ◽  
S.-i. Hoshino ◽  
O. Hazeki ◽  
...  
Keyword(s):  
Cell Lines ◽  
Myeloid Cell ◽  
Chemotactic Peptide ◽  
Superoxide Generation

Chemotactic peptide-induced exocytosis in neutrophils: granule fusion patterns depend on the source of messenger calcium

1986 ◽  
Vol 83 (1) ◽  
pp. 293-311
Author(s):  
D.E. Chandler ◽  
C.J. Kazilek
Keyword(s):  
Intracellular Calcium ◽  
Cytochalasin B ◽  
Freeze Fracture ◽  
Extracellular Calcium ◽  
Chemotactic Peptide ◽  
Compound Exocytosis ◽  
Cell Centre ◽  
Peripheral Cytoplasm

Rabbit neutrophils, exposed either to partially purified human C5a or to formylmethionyl-leucyl-phenylalanine in the presence of 5 micrograms ml-1 cytochalasin B underwent a rapid, compound exocytosis. The pattern of granule fusion, as visualized in freeze-fracture replicas, differed depending on the source of messenger calcium. In the presence of extracellular calcium, a linearly directed pattern, consisting of finger-like invaginations converging at the cell centre, was prominent at 10–20 s after stimulation. After stimulation for 20–40 s, further fusion of granule membranes created extremely convoluted surfaces, some consisting of up to a dozen granule membranes connected by narrow pores or flat ribbons of membrane. In many cells the peripheral cytoplasm was constricted to form lobes or finger-like protrusions. Neutrophils stimulated in the absence of extracellular calcium exhibited granule fusion in the directed pattern, with only occasional involvement of the convoluted patterns seen when calcium is present. In contrast, neutrophils depleted of intracellular calcium before stimulation (and thereby forced to use extracellular calcium for triggering secretion) exhibited the convoluted pattern of granule fusion almost exclusively. These results suggest that the directed pattern of fusion is initiated by release of intracellular calcium or a calcium-independent pathway and that the non-directed, convoluted pattern of fusion is initiated by entry of extracellular calcium.

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