Cytokineplasts from human blood polymorphonuclear leukocytes lack of oxidase activity and extended functional longevity

Cytokineplasts (CKPs) are membrane-bounded, anucleate, granule-poor cytoplasmic fragments, induced from PMNs by brief heat (45 degrees C, 9 min), which retain motile function including chemotaxis and phagocytosis. CKPs can respond to repeated chemotactic stimuli even after having been held overnight...

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Bibliographic Details
Published in:Inflammation 1985-03, Vol.9 (1), p.99-106
Main Authors: MALAWISTA, S. E, VAN BLARICOM, G, CRETELLA, S. B
Format: Article
Language:English
Subjects:
Biological and medical sciences
Cell physiology
Cell Survival
Cytoplasm - enzymology
Cytoplasm - ultrastructure
Fundamental and applied biological sciences. Psychology
Hot Temperature
Humans
Miscellaneous
Molecular and cellular biology
Neutrophils - enzymology
Neutrophils - ultrastructure
Oxidoreductases - metabolism
Time Factors
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Summary:Cytokineplasts (CKPs) are membrane-bounded, anucleate, granule-poor cytoplasmic fragments, induced from PMNs by brief heat (45 degrees C, 9 min), which retain motile function including chemotaxis and phagocytosis. CKPs can respond to repeated chemotactic stimuli even after having been held overnight at room temperature, and hence "outlive" control PMNs. We now report that adherent CKPs lack significant oxidase activity, as measured by reduction of nitroblue tetrazolium (NBT) dye, (1) 5 min after heat, when they are often still attached to their parent PMNs (which generally do not reduce NBT either); (2) later on, when they are free; and (3) when cells have been pretreated on endotoxin-coated substrata or with phorbol myristate acetate (PMA); both pretreatments cause the large majority of adherent control PMNs to reduce NBT. Moreover, cells harvested from glass just after heat lack the normal increase in oxygen consumption seen on stimulation with PMA or with heat-killed staphylococci. PMA-stimulated respiratory burst activity was not restored to heated cells by exogenous NADPH. Thus, heat applied to normal PMNs can dissociate motile function from oxidase activity; in this respect CKPs resemble PMNs in chronic granulomatous disease. The apparent increased functional stability of CKPs may indicate that normal PMNs are not immune to their own oxidative killing mechanism.
ISSN:0360-3997
1573-2576
DOI:10.1007/BF00915416