Abstract

In an experiment in which Trypanosoma cruzi was inoculated into the peritoneum of immune and normal mice, the parasites were found in blood of normal mice within 2 hr, but few or none were found in blood of immune animals during the experiment. Immunized rats gave the same response to intraperitoneally inoculated Trypanosoma lewisi, and this parasite was used in the study of the response. The response was not peculiar to the immunity of rats and mice to trypanosomes. Rat blood (labeled with Plasmodium berghei) was found in the blood of normal mice within 2 hr after intraperitoneal inoculation, but was not found in blood of mice previously sensitized with normal rat blood 6 hr after inoculation. Mice (as well as rats) passively immunized with anti-T. lewisi rat serum inhibited the passage of T. lewisi to the blood after intraperitoneal inoculation. When P. berghei-infected mouse blood was inoculated along with trypanosomes into the peritoneal cavity of passively immunized mice, P. berghei-infected cells, but not trypanosomes, were found in the blood within 2 hr. Thus, the failure of antigen (trypanosomes or erythrocytes) to pass from peritoneal cavity to blood of immunized animals does not seem to be attributable to occluded passageways, or to the alteration of sensitized tissues by antigen, and it was shown that the response was specific for the immunizing antigen. Examination of T. lewisi recovered from the peritoneal cavity of immune and normal rats during a 4-hr period after inoculation indicated that the trypanosomes from immune rats were not killed, immobilized, agglutinated, or phagocytized. The mechanism that prevented passage of trypanosomes from the peritoneal cavity to the blood of immune rats or mice was not apparent. However, it is suspected that this response might be an allergic or sensitivity reaction of sensitized tissue to antigen. It has been observed in this laboratory that Trypanosoma cruzi did not appear in the blood of mice that had recovered from T. cruzi infection after intraperitoneal inoculation, but were present in the blood of normal mice within 2 hr. It seemed that here was a concise measurement of the acquired immunity to a protozoan parasite, and attempts were made to measure the acquired immunity of rats and mice to Plasmodium berghei in this manner. In these experiments it was observed that P. berghei parasites passed from the peritoneal cavity into the blood of immune animals as readily as in normal rats and mice. The experiments indicated that this observation was not attributable to quantitative difference in degree of immunity, nor to the intracellular nature of P. berghei parasites. This obvious difference in the immune responses of rats and Received for publication 20 August 1963. * This work was supported in part by United States Public Health Service Grant AI-13135-04. mice strongly suggested that their immunity to T. cruzi and P. berghei might be based on different mechanisms (Cox, 1963). In further study of this immune response to trypanosomes, it was found that rats that had recovered from Trypanosoma lewisi infection behaved as did mice recovered from T. cruzi after intraperitoneal inoculation of parasites. T. lewisi was not found in the blood of rats that had recovered from infection with this trypanosome, but was demonstrated in blood of normal rats within 2 hr after intraperitoneal inoculation with parasites. This observation on the immune response of rats to T. lewisi has been previously studied. Rabinowitsch and Kempner (1898) observed that T. lewisi incubated with serum of recovered rats did not appear in the blood of normal rats after intraperitoneal inoculation. Laveran and Mesnil (1901) found that the parasites would not pass from peritoneal cavity to blood of actively or passively immunized rats. They reported that phagocytic activity

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