Ingestion of yeast forms of Sporothrix schenckii by mouse peritoneal macrophages.

The ingestion by thioglycolate-elicited mouse peritoneal macrophages of yeast forms of two strains of Sporothrix schenckii was studied. Yeast forms opsonized with concanavalin A (ConA) were extensively phagocytized, and the phagocytic indexes depended on the concentration of ConA and apparently on the number of lectin receptors at the yeast surface as well. Neuraminidase treatment of S. schenckii increased the ingestion of unopsonized yeasts 7.7-fold. The addition of monosaccharides and derivatives partially inhibited phagocytosis. Mannose, rhamnose, and galactose, which are major constituents of S. schenckii surface antigens, reduced the phagocytic indexes by 40 to 50%. Glucosamine, N-acetylglucosamine, and N-acetylneuraminic acid were equally effective as inhibitors of phagocytosis. A mixture of five neutral sugars and glucosamine inhibited phagocytosis by 73%. The inhibitory effect of simple sugars could be amplified by using neuraminidase-treated yeast cells. Pentoses and glucose were inactive or slightly inhibitory. A purified rhamnomannan inhibited phagocytosis of the homologous strain, whereas partially purified peptidopolysaccharides were toxic to peritoneal macrophages. A partially purified galactomannan from S. schenckii was inhibitory (62% inhibition), and a peptidopolysaccharide fraction in which the O-linked carbohydrate chains had been removed neither was toxic to macrophages nor inhibited phagocytosis. Pretreatment of macrophages with simple sugars under conditions inhibiting ingestion or binding of S. schenckii did not affect phagocytosis of latex particles or sensitized sheep erythrocytes. The presence of receptors at the peritoneal macrophages which bind S. schenckii cell surface components is suggested.

Phagocytosis of Herpetomonas samuelpessoai by mouse peritoneal macrophages: effect of lidocaine, concanavalin A and carbohydrates.

Normal mouse peritoneal macrophages, as well as macrophages treated with Concanavalin A (Con A) and lidocaine, were incubated in the presence of normal, Con A-treated or glutaraldehyde-fixed Herpetomonas samuelpessoai. The percentage of infected macrophages, the mean number of protozoa per macrophage and the phagocytic index was determined after 1 and 2 h of protozoa-macrophage interaction. The uptake of H. samuelpessoai by the macrophages was increased when either the protozoa or the macrophages or both were treated with Con A. The effect of Con A was dependent on its concentration and was inhibited by alpha-methyl-D-mannoside. The uptake of H. samuelpessoai by macrophages was significantly inhibited by xylose, mannose and a polysaccharide isolated from the portozoan. Lidocaine-treated macrophages incorporated less protozoa than normal macrophages. Both Con A and lidocaine induced the formation of a large number of cytoplasmic vacuoles in the macrophages. Glutaraldehyde-fixed protozoa were more easily incorporated by the macrophages than living cell. However, their uptake was not stimulated by treatment of the macrophages with Con A.

Phagocytosis of the three developmental forms of Trypanosoma cruzi: effect of specific sera.

Studies were carried out aiming at comparing the uptake of the three evolutionary stages of Trypanosoma cruzi by mouse peritoneal macrophages, influenced by specific immunosera. Incorporation of T. cruzi by macrophages was time dependent. In absence of antibody, trypomastigotes are forms more effectively incorporated by macrophages. Pre-incubation of macrophages with specific sera against each of the T. cruzi morphological stages was followed by an increase in the uptake of amastigotes and trypomastigotes but not of epimastigotes. Our results show that amastigotes, in comparison with the other T. cruzi forms are more actively phagocytized in presence of specific serum.