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Murine Malaria: The Role of Humoral Factors and Macrophages in Destruction of Parasitized Erythrocytes¹

Departments of Microbiology and Medicine, Baylor College of Medicine, and the Immunology Research Laboratories of the Methodist and Veterans Administration Hospitals, Houston, Texas

Abstract

Interactions between cellular and humoral factors in the response of mice to malaria were evaluated by placing Millipore diffusion chambers (0.22 µ pore size) containing washed macrophages from mice and mouse erythrocytes parasitized with Plasmodium berghei in the peritoneal cavities of BALB/c^- male mice that were normal or had acute or chronic malaria. Macrophages were obtained from normal mice, endotoxin-treated mice, quinacrine-treated mice, or mice with chronic malaria established by treatment with quinacrine hydrochloride. Parasitized erythrocytes were obtained from mice with acute malaria. The rate of destruction of parasitized erythrocytes alone in Millipore chambers was greater when chambers were placed in mice with chronic malaria than when placed in normal mice. This finding suggested that humoral factors diffused into the chamber causing increased destruction of parasitized erythrocytes. When macrophages from mice with chronic malaria were added to the chambers with parasitized erythrocytes, and implanted into normal mice, an enhanced rate of clearance of parasitized erythrocytes also occurred. Macrophages from normal mice or from endotoxin-treated mice did not increase the rate of clearance of parasitized erythrocytes when placed in normal mice. However, an accelerated rate of clearance of parasitized erythrocytes occurred when chambers containing parasitized erythrocytes and macrophages from normal mice or mice with chronic malaria were placed into mice with chronic malaria. Therefore, humoral factors not only acted directly on the chamber contents to cause destruction of parasites, but also possibly acted synergistically with macrophages to enhance destruction of parasitized erythrocytes.

Footnotes

¹ This work was taken in part from a dissertation submitted by B.S.C. in partial fulfillment of the requirements for the degree of Doctor of Philosophy. This study was supported in part by Research Grants HE 05435 and RR 00350, by Training Grant AI 00325 from the National Institutes of Health, by the Veterans Administration and by Grant NGR 44-003-044 from the National Aeronautics and Space Administration. B.S.C. was the recipient of Public Health Service Fellowship GM 42054 of the National Institute of General Medical Sciences.

² Address requests for reprints to William T. Butler, M.D., Immunology Research Laboratory, Veterans Administration Hospital, Houston, Texas 77031.