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Biomedical subjects

C E Tanner

Publications and source records attributed to C E Tanner.

At least 37 records · Page 2Linked to original sources

Susceptibilities of macrophage populations to infection in vitro by Leishmania donovani.

Many studies have demonstrated differences in the resistance of strains of mice to infection by Leishmania donovani, Salmonella typhimurium, and Mycobacterium bovis BCG; this resistance/susceptibility phenotype seems to be controlled by a single gene. The present study investigated the susceptibility of liver, lung, peritoneal, and spleen macrophages to infection by L. donovani promastigotes in vitro; the objective was to determine if the susceptibility of animals was expressed by their macrophages when infected in vitro. This study indicated that the Lsh phenotype was only expressed by liver macrophages. The liver macrophages of the susceptible C57BL/6J strain were significantly more phagocytic than those of the resistant C57L/J strain; infection affected the phagocytic activity of the macrophage population. These results indicated that only liver macrophages can express the Lsh gene. Recognition of expression is in part due to its effect on the phagocytic activity of the macrophages.

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Echinococcus multilocularis: responses to infection in Mongolian gerbils.

Mongolian gerbils (Meriones unguiculatus) inoculated intraperitoneally with three acephalic cysts of Echinococcus multilocularis were very susceptible to infection. Aspects of the responses of gerbils to this infection were examined to determine if they could be related to the progress of the infection. Hematologic changes observed during the infection included anemia, reticulocytosis, lymphocytopenia, neutrophilia, monocytosis, and eosinopenia; these changes were related to the size of the infection. Infected gerbils also produced specific protein-A binding antibodies to E. multilocularis. At 14 weeks after inoculation, infected gerbils showed splenomegaly and somewhat elevated serum transaminase levels, although serum 5'-nucleotidase levels were normal.

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Protection against experimental echinococcosis by non-specifically stimulated peritoneal cells.

Infection of cotton rats with Echinococcus multilocularis or vaccination with BCG, or its cell walls, activates peritoneal cells to kill the protoscolices of the parasite in vitro and protects laboratory animals against the cestode. To determine whether other 'non-specific' stimuli would also protect against the parasite, cotton rat peritoneal cells were activated in vivo with PHA and transferred to recipients 3 days later. The recipients, controls and PHA-treated animals were then inoculated with the parasite; 3 days after inoculation other untreated infected animals received cells activated in vivo with PHA. PHA-activated cells, the PHA treatment itself and immunization with a homogenate of the parasite stimulated a leucocytosis and protected against infection by E. multilocularis; carrageenan abrogated protection in PHA-treated animals. The results of this study confirm that protection against echinococcosis can be induced non-specifically; these results suggest that immunity in hydatid disease may have an important component in the inflammatory reaction.

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The depressed response of spleen cells from rats infected by Trypanosoma lewisi in producing a secondary response in vitro to sheep erythrocytes and the ability of soluble products of the trypanosome to induce this depression.

The non-pathogenic Trypanosoma lewisi depresses the ability of infected rat spleen cells to respond immunologically to sheep erythrocytes. A study was made to determine whether the parasite would produce this same phenomenon in vitro in Marbrook culture vessels with erythrocyte-primed spleen cells from normal rats; the antibody response of the spleen cells was measured by the plaque-forming cell assay. Soluble factors from 1 X 10(7) T. lewisi depress the ability of primed cells to form a secondary antibody response in vitro to sheep red cells. The intensity of the inhibitory activity depends on the stage of the life cycle of the parasite and can also be demonstrated using sonicated, frozen-thawed or boiled preparations of the organism. It is suggested that the immunodepressive substances may be a glycoprotein and that it (they) may arise both from the intracellular and from the extracellular compartments of the organism. It is likely that the host-parasite associations in trypanosomiasis are regulated by such soluble parasite factors.

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The nonrandom, negative binomial distribution of experimental trichinellosis in rabbits.

The distribution of parasite populations in their hosts has been the subject of a number of mathematical analyses and it has been found that these distributions are generally nonrandom and overdispersed. Data on the recovery of Trichinella spiralis in the laboratory from 371 outbred rabbits were examined. The distribution of their parasite burden was overdispersed and best fit by a negative binomial frequency distribution. The intensity of the infections was almost totally independent of the dose of inoculation, the duration of the infection, and the weight of the animals; the variations within the replicate counts were small and normally distributed about their means. These results indicate that nonrandom overdispersion may be a characteristic of even carefully controlled laboratory infections, and susceptibility factors should be considered seriously in mathematical models of parasites.

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Protection of cotton rats against experimental Echinococcus multilocularis infections with BCG cell walls.

Previous works has indicated that cotton rats treated with Mycobacterium bovis strain BCG are effectively protected against an infection with the metastatically proliferating metacestodes of Echinococcus multilocularis. In an attempt to induce a similar protection in the absence of tubercular granulomatous lesions, cotton rats were treated with BCG cell walls. A single injection of 150 micrograms of cell walls, emulsified in mineral oil-Tween-saline, 2 weeks before the inoculation of the parasite completely protected the animals against infection with E. multilocularis. This protection was correlated with an increase in the numbers of monocytes and, as judged by acid phosphatase activity, an activation of these cells. This study shows that BCG cell walls are as effective in protecting animals against E. multilocularis as the viable organism.

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Immunoprophylaxis with BCG of experimental Echinococcus multilocularis infections.

Previous studies have demonstrated that prophylactic treatment with BCG protects cotton rats (Sigmodon hispidus) against experimental infections with Echinococcus multilocularis; this treatment can, however, induce granulomatous reactions. In an attempt to identify a minimum prophylactic dose of BCG which would not induce granulomas, cotton rats were treated intraperitoneally with various doses of BCG (10(1) to 10(7) colony-forming units [CFU]) and then inoculated intraperitoneally with one brood capsule of the parasite. Consistent and complete protection was obtained by the inoculation of as few as 10(3) CFU of BCG. A dose of 10(1) CFU gave no protection whatsoever, and 10(2) CFU gave only partial protection. Doses larger than 10(3) (10(5), 10(7) CFU) also afforded complete protection but gave rise to granulomatous lesions. At the time of the inoculation of the parasite, protection coincided with a general elevation of leukocytes, especially cells of the monocyte/macrophage series. It is proposed that these results support evidence for the macrophage being the principal potential effector cell in hydatid disease.

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Host serum proteins in Echinococcus multilocularis: complement activation via the classical pathway.

The presence of host serum proteins, including IgG and IgM, within the cyst membranes and on the surface of protoscoleces of Echinococcus multilocularis was demonstrated by the use of HRPO-conjugated purified antisera. Viable protoscoleces incubated either in EDTA- or EGTA-fresh human sera were not lysed; the addition of calcium restored the protoscolecidal activity of the EGTA serum. It is concluded that the complement-mediated lysis of this metazoan organism proceeds via the classical pathway of complement activation. The results are discussed in relation to the ability of this parasite to survive in the immunologically hostile environment of the host.

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