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From The Johns Hopkins University School of Medicine at The Good Samaritan Hospital, Clinical Immunology Division, 5601 Loch Raven Boulevard, Baltimore, MD 21239
Abstract
Phagocytosis was found to stimulate ECF release from neutrophils (PMN). Human PMN (
; 98%) were exposed to zymosan (Z), zymosan-coated with complement (Z(x)), or zymosan in the presence of serum (Z(s)). The release of ECF was shown to be time- and dose-dependent. Like ionophore-induced ECF, phagocytosis-derived ECF preferentially attracted and deactivated eosinophils. Chromatography on Sephadex G-25 revealed an elution pattern similar to the antigen-induced, basophil-derived and to the ionophore-induced PMN-derived ECF. The addition of complement either as Z(x) or Z(s) accelerated the release of ECF. With both stimuli, the initial kinetics of ECF paralleled the release of
-glucuronidase and NBT reduction. With Z alone,
-glucuronidase release and NBT reduction were negligible, whereas the amount of ECF released was similar to that induced by Z(x). In the presence of serum Z(s), decreased activity was noted. Supernatants of phagocytosis at late time periods showed less activity than early supernatants, suggesting that ECF might be inactivated. These data indicate that phagocytosis causes the release of an ECF, which appears to be similar to the IgE-induced ECF-A.
Footnotes
1 This work was supported by Grants 07290 and 08270 from the National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland. This is publication No. 229, O'Neill Research Laboratories, The Good Samaritan Hospital.
2 Recipient of the Stetler Research Fund for Women Physicians.
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