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Previous work (1)(1) has shown that normal human eosinophils show a preferential capacity, in comparison with neutrophils, to bind to antibody- coated schistosomula of Schistosoma mansoni. This effect is attributable to a temperature-dependent function of the eosinophil which renders its binding stable and irreversible by aggregated gamma globulin or Staphylococcus aureus protein A. In contrast, the binding of neutrophils is readily reversible by these agents. It has now been shown that the differences observed between eosinophils and neutrophils is a property of their interaction with living schistosomula. When dead or artificially damaged schistosomula were tested, neutrophils showed a markedly enhanced capacity to adhere, in both the presence and absence of anti-chistosomular serum. Subsequent experiments were designed to test the hypothesis that the strong, stable binding of eosinophils was attributable to degranulation, with release of granule contents which would then serve as ligands to bind the cell to the organism. First, an enhanced adherence both of eosinophils and of neutrophils could be demonstrated in the presence of eosinophil major basic protein (MBP) or of protamine, a high molecular weight cation. Second, the binding of eosinophils induced by concanavalin A (Con A) was found to differ markedly from that induced by antischistosomular serum. Con A-mediated binding of eosinophils was fully reversible by alpha-methyl-mannoside, was not associated with damage to the organism, and did not lead to degranulation of the cell, as estimated by measuring the release of MBP into the culture supernate. However, induction of degranulation of concanavalin A-bound eosinophils, but not of neutrophils, with the calcium ionophore A23187 converted the reaction into one which was no longer reversible by alpha- methylmannoside and in which damage to the organism now did occur. These findings support the hypothesis that the stable binding of eosinophils is associated with degranulation, a process which may contribute to the preferential capacity of this cell to mediate antibody-dependent damage to schistosomula.
A E Butterworth, and
M A Vadas, and
D L Wassom, and
A Dessein, and
M Hogan, and
B Sherry, and
G J Gleich, and
J R David
February 1979,
Journal of immunology (Baltimore, Md. : 1950),
A E Butterworth, and
M A Vadas, and
D L Wassom, and
A Dessein, and
M Hogan, and
B Sherry, and
G J Gleich, and
J R David
January 1977,
The Journal of experimental medicine,
A E Butterworth, and
M A Vadas, and
D L Wassom, and
A Dessein, and
M Hogan, and
B Sherry, and
G J Gleich, and
J R David
March 1990,
Immunology,
A E Butterworth, and
M A Vadas, and
D L Wassom, and
A Dessein, and
M Hogan, and
B Sherry, and
G J Gleich, and
J R David
May 1987,
Journal of immunology (Baltimore, Md. : 1950),
A E Butterworth, and
M A Vadas, and
D L Wassom, and
A Dessein, and
M Hogan, and
B Sherry, and
G J Gleich, and
J R David
July 1985,
The American journal of tropical medicine and hygiene,
A E Butterworth, and
M A Vadas, and
D L Wassom, and
A Dessein, and
M Hogan, and
B Sherry, and
G J Gleich, and
J R David
January 1982,
Cellular immunology,
A E Butterworth, and
M A Vadas, and
D L Wassom, and
A Dessein, and
M Hogan, and
B Sherry, and
G J Gleich, and
J R David
July 1977,
Federation proceedings,
A E Butterworth, and
M A Vadas, and
D L Wassom, and
A Dessein, and
M Hogan, and
B Sherry, and
G J Gleich, and
J R David
December 1978,
Journal of immunology (Baltimore, Md. : 1950),
A E Butterworth, and
M A Vadas, and
D L Wassom, and
A Dessein, and
M Hogan, and
B Sherry, and
G J Gleich, and
J R David
June 1989,
Journal of immunology (Baltimore, Md. : 1950),
A E Butterworth, and
M A Vadas, and
D L Wassom, and
A Dessein, and
M Hogan, and
B Sherry, and
G J Gleich, and
J R David
March 1981,
Journal of immunology (Baltimore, Md. : 1950),
