The JI
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     
 


The Journal of Immunology, 1976, 117: 235-241.
Copyright © 1976 by The American Association of Immunologists, Inc.

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by König, W.
Right arrow Articles by Lichtenstein, L. M.
Right arrow Search for Related Content
PubMed
Right arrow Articles by König, W.
Right arrow Articles by Lichtenstein, L. M.

Eosinophil Chemotactic Factor (ECF)

II. Release from Human Polymorphonuclear Leukocytes During Phagocytosis1

Wolfgang König, Beate M. Czarnetzki2 and Lawrence M. Lichtenstein

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 ({tau}; 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 beta-glucuronidase and NBT reduction. With Z alone, beta-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.




This article has been cited by other articles:


Home page
Infect. Immun.Home page
F. H. Falcone, A. G. Rossi, R. Sharkey, A. P. Brown, D. I. Pritchard, and R. M. Maizels
Ascaris suum-Derived Products Induce Human Neutrophil Activation via a G Protein-Coupled Receptor That Interacts with the Interleukin-8 Receptor Pathway
Infect. Immun., June 1, 2001; 69(6): 4007 - 4018.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1976 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1976 by The American Association of Immunologists, Inc. All rights reserved.