THE mechanism of cell destruction in allergic inflammation is not well understood. Two explanations for production of cell damage have, however, been proposed: (a) that the antigen-antibody reaction causes, in some non-specific manner, permeability changes in cells which result in the release of active mediators of inflammation (histamine, etc.) and that the latter are directly involved in the allergic process1; (b) that the antigen-antibody reaction activates proteolytic enzymes (plasmin, proteases) that injure the cells2–4.

SEVERAL studies were undertaken in order to reproduce in laboratory animals cardiac lesions which would resemble those appearing in human beings suffering from the sequelae of streptococcal infections (Schultz, 1936 ; Smith, Morgan and Mudd, 1940; Gross, Cooper and Philips, 1941; Robinson, 1947; Schultz, 1947; Murphy and Swift, 1949; Murphy, 1949; Clawson, 1950; Robinson, 1951; Murphy, 1952; Glaser, Thomas, Morse and Darnell, 1956). These studies describe the histopathological changes obtained in laboratory animals following inoculation by various routes of haemolytic streptococci, of their products and of a number of other micro-organisms. As to the mechanism involved in the production of cardiac lesions, two main theories have been proposed: (a)allergic phenomena,or production ofa uto- antibodies to the heart muscle (Rich and Gregory,1944; Rich,1946; Cavelty, 1947a and 1947b), (b) direct action of haemolytic streptococci and their toxins on the heart muscle (McLeod, 1953; Kellner and Robertson, 1954a and 1954b). Although both theories have been supported by some experimental evidence, the exact mechanism has not yet been clarified. This study describes the histo-pathological changes obtained in rabbits as a result of single intramyocardial injections of haemolytic streptococci and their cell-free extract, as well as of other bacterial species, both related and not related to haemolytic streptococci. The possible mechanism involved, and especially the role of trauma to the myocardium, in inducing cardiac lesions, is described.

STUDIES on the cytotoxic action of antibodies, plasmin and streptococcal haemolysins on Ehrlich ascites tumour cells (E-cells) have been recently described (GCinsburg, 1959; Ginsburg and Grossowicz, 1960; Ginsburg and Ram, 1960). It was found that the cytopathogenic changes induced in the tumour cells by streptococcal haemolysins were morphologically very similar to those caused by anti-Ehrlich ascites tumour rabbit serum (AE), the action of the latter is known to be complement dependent (Flax, 1956; Goldberg and Green, 1959). It is known that both the haemolytic as well as the cytopathogenic effect caused by streptococcal haemolysins can be inhibited by antihaemolytic agents such as cholesterol, lecithin, congo red and trypan blue (Van Heyningen, 1950; Bernheimer, 1954; Ginsburg, 1959; Ginsburg and Grossowicz, 1960). On the other hand, the cytotoxic and haemolytic effect of antibodies can be inhibited by agents known to destroy or inhibit complement action, chelating agents, plasmin, heparin etc. (Gorrill and Hobson, 1952; Pillemer, Ratnoff, Blum and Lepow, 1953; Mayer, 1 958; Ginsburg and Ram, 1960). The present study shows that the cytotoxic action of antibodies produced in the rabbit against Ehrlich ascites tumour cells can be inhibited by various phospholipids and some of their constituents as well as by agents known to inhibit streptococcal haemolysins. In addition the inhibition of immune haemolysis by phospholipids will be described.