Introduction Cationic polyelectrolytes play important roles in many biological systems. Histones [20] and cationic proteins of lysosomal origin [8, 18, 24, 25, 28, 33, 36, 37], both rich in arginine, and synthetic poly a-amino acids [3, 4, 5, 6, 23, 30] have been shown to be bactericidal and cytotoxic to a variety of bacteria and mammalian cells. In addition, these compounds modulate blood coagulation [30] and fibrinolysis [10]; agglutinate bacteria and mammalian cells [30]; modulate chemotaxis [16]; enhance adherence of mammalian cells to surfaces [26]; function as opsonins for phagocytosis by both "professional" and "nonprofessional" cells [3,5,6,17,27,28,34]; activate autolytic cell wall enzymes of Staphylococci [15]; and block Fe receptors for IgG upon certain group A Streptococci [14]. More recent studies have shown that histone-opsonized bacteria induced intense Iuminot- dependent chemiluminescence (LDCL) in human polymorphonuclear leukocytes (PMNs) and mouse peritoneal macrophages [In Furthermore, poly-i.-arginine collaborated with mixtures of lectins, calcium ionophore and the chemotactic peptide formyl-methionyl-Ieucyl-phenylalanine to induce synergistic LDCL and superoxide production in human PMNs [12,13]. Thus, arginine-rich polyelectrolytes appear to participate in many cellular functions related to host defenses against infection, presumably by mechanisms involving electrostatic interactions and ligand- receptor coupling phenomena. The objective of this present study was to investigate the possibility that arginine- rich polycations might facilitate the introduction of a variety of agents into eukaryotic cells. For this purpose, we have studied phagocytosis by Entamoeba histolytica of Candida albicans, and by Acanthamoeba palestinensis of Mycobacterium marinum.

Introduction. Although a voluminous literature exists today which describes, in great detail, the role played by "professional" phagocytes and by serum components in the killing of pathogenic bacteria in vitro and in vivo (l-7) very surprisingly, however, little is actually known about the fate and mode of disposal of microorganisms once they had been rendered non-viable by the defence systems of the host. It is expected that the rich arsenal of lysosomal hydro- lases, including the key muralytic enzyme lysozyme (LYZ), present in leukocytes and in body fluids might be adequate to biodegrade the complex structures of the microbial cells. Paradoxically, however, the majority of bacteria are highly refractory to LYZ action. There is also some confusion in the literature concerning the distinction between bactericidal and bacteriolytic processes. It is conceivable that while a major degradation of microbial cell walls may be followed by a bactericidal reaction, the mere killing of bacteria either by oxygen radicals (2) or by complement-dependent cytlytic antibodies (7) may not necessarily be accompanied by a significant cell wall degradation. Many experimental models, with laboratory animals, have distinctly shown the persistence, for very long periods, of non-viable bacteria and of undergraded microbial cell wall components, within macrophages, in chronic inflammatory sites (8-l8). Thus, one should categorically differentiate between bactericidal and bacteriolytic phenomena. It is apparent, therefore, that mammalian tissues fail, for still not/fully known reasons, to biodegrade and eliminate microbial cell wall components. Peptidoglycan (PPG)-polysaccharide (PS) complexes derived from microbial cell walls possess distinct pathobiological and and pathophysiological properties (19-21). These include the capacity to activate the complement cascade and to generate chemotactic agents, to induce fever, to activate the respiratory burst in leukocytes and to modulate the immune responses (19-24), to mention only a few of the plethora of functions ascribed to PPG. These properties may also explain the very complex interrelationships which exist between the parasite and the host during microbial infections and the possible reasons for the development of certain post-infectious sequelae, which involve the prolonged persistence of bacterial cell wall components in tissues (10-15).

Liquoid (polyanethole sulfonate) was neither capable of influencing the growth nor the viability of staphylococci. But liquoid induced a suppression of the activity of different autolytic wall systems of normally growing staphylococci, i.e., autolysins which participate in cross wall separation as well as autolysins which are responsible for cell wall turnover. Additionally, the lysostaphin-induced wall disintegration of staphylococci was inhibited by liquoid. However, no indication could be found for a direct inhibition of lytic wall enzymes by liquoid; rather an interaction of liquoid with the target structure for the autolytic wall enzymes, the cell wall itself, was postulated. On the basis of the experimental data with the teichoic acid- mutant S. aureus 52A5 the sites of wall teichoic acid were supposed to be an important target for the binding of liquoid to the staphylococcal cell wall.