The Journal of Experimental Medicine
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The Journal of Experimental Medicine, Vol 117, 647-661, Copyright ©, 1963, by The Rockefeller Institute


ARTICLE

A HEMOLYTIC SYSTEM ASSOCIATED WITH ENTERITIS IN RABBITS : I. NATURE OF THE CELL CHANGE AND THE SERUM FACTORS CONCERNED



Robert S. Evans M.D.1, Margaret Bingham M.D.1, and Russell S. Weiser Ph.D.1

1 From the Medical Service, Veterans Administration Hospital and the Department of Microbiology, University of Washington School of Medicine, Seattle

A disease characterized by frequent association of enteritis and polyagglutinable cells often develops in weanling rabbits. The red cell lesion renders the cells susceptible to agglutination and hemolysis in normal rabbit sera. The degree of red cell abnormality varies among different animals and disappears when the animals recover.

The abnormality of the red cells responsible for their polyagglutinability and susceptibility to hemolysis was resistant to the action of trypsin or papain and persisted in heated stroma preparations derived from polyagglutinable cells.

The factors necessary for agglutination and hemolysis of the polyagglutinable cells are present in normal rabbit sera but are lacking in the sera of affected rabbits. These factors returned to normal levels as the polyagglutinable cell lesion disappeared. The sera of rabbits with polyagglutinable cells contained normal levels of complement and properdin.

Whereas the agglutinating factor in normal sera is heat-stable at 56°C for 30 minutes, the hemolytic factor is heat labile. The hemolytic factor is apparently distinct from complement and properdin since it was adsorbed from normal rabbit serum by zymosan or by polyagglutinable cells at 0°C. However, complement was fixed when normal rabbit serum was reacted with stroma from polyagglutinable cells.

Hemolysis of polyagglutinable cells by normal rabbit serum at 25°C was inhibited by preliminary incubation of the mixture at 0°C prior to incubation at 25°C. Evidence was obtained which indicated that this inhibition was due to progression of a reaction involving Ca++ independent of a reaction involving Mg++.

Submitted on November 6, 1962


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