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The immunosuppressant effect of T. lewisi infection on the multiplication of T. gondii was compared in peritoneal (MP) and alveolar macrophages (MA) of white rat. Two animal groups were infected with T. lewisi and sacrificed after four days and seven days post infection. A group without infection was maintained as a control. The number of intracellular parasites (tachyzoites) (IT) was counted by light microscopy, calculating the rate infection rate per 100 total cells (TC) and per infected cells (IC) for each group of phagocyte cells. The relation quotient IT, TC or IC multiplied percent, provided a statistical ratio (RE) of the relative number of parasites in both cellular types for each time interval. MA as well as MP obtained after 4 days showed a significant increase in the multiplication of T. gondii with respect to the control. Unlike the MP (which had an increase in the multiplication of T. gondii the fourth day of infection with T. lewisi diminishing towards the seventh day), the MA had an increase in the multiplication of the parasite from the fourth to the seventh day. This difference can be related to the route of infection used for the experiments, that affect the MP directly with a greater effect in comparison with the MA of the lungs. Lung compartment will be affected later, when the infection becomes systemic between the fourth and sixth day of infection. The immunity against T. gondii is similar between both phagocytes, but the time of infection and the compartment where the cells are located, makes the difference in the response time against T. gondii. Supernatants from macrophage cultures or T. lewisi by rat did not induced any immunosuppression.

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The immunosuppressant effect of T. lewisi (Kinetoplastidae) infection on the multiplication of Toxoplasma gondii (Sarcocystidae) on alveolar and peritoneal macrophages of the white rat. The immunosuppressant effect of T. lewisi infection on the multiplication of T. gondii was compared in peritoneal (MP) and alveolar macrophages (MA) of white rat. Two animal groups were infected with T. lewisi and sacrificed after four days and seven days post infection. A group without infection was maintained as a control. The number of intracellular parasites (tachyzoites) (IT) was counted by light microscopy, calculating the rate infection rate per 100 total cells (TC) and per infected cells (IC) for each group of phagocyte cells. The relation quotient IT, TC or IC multiplied percent, provided a statistical ratio (RE) of the relative number of parasites in both cellular types for each time interval. MA as well as MP obtained after 4 days showed a significant increase in the multiplication of T. gondii with respect to the control. Unlike the MP (which had an increase in the multiplication of T. gondii the fourth day of infection with T. lewisi diminishing towards the seventh day), the MA had an increase in the multiplication of the parasite from the fourth to the seventh day. This difference can be related to the route of infection used for the experiments, that affect the MP directly with a greater effect in comparison with the MA of the lungs. Lung compartment will be affected later, when the infection becomes systemic between the fourth and sixth day of infection. The immunity against T. gondii is similar between both phagocytes, but the time of infection and the compartment where the cells are located, makes the difference in the response time against T. gondii. Supernatants from macrophage cultures or T. lewisi by rat did not induced any immunosuppression. Rev. Biol. Trop. 57 (1-2): 13-22. Epub 2009 June 30.

El efecto inmunosupresor de la infección de T. lewisi sobre la multiplicación de T. gondii fue comparado en macrófagos peritoneales (MP) y alveolares (MA) de rata. El número de parásitos (taquizoitos) intracelulares (TI) fue contado por microscopía de luz. Los macrófagos alveolares y peritoneales (MP) de animales con 4 días de infección con T. lewisi muestran un aumento significativo en la multiplicación de T. gondii. A diferencia de los MP (que muestran un aumento en la multiplicación de T. gondii al cuarto día de infección con T. lewisi disminuyendo hacia el séptimo día), los MA mantienen un aumento en la multiplicación del parásito desde el cuarto, aumentando hacia el séptimo día de infección. Esta diferencia se puede deber a la ruta de infección utilizada para los experimentos que afectan directamente los MP donde se observa un efecto mayor y más temprano en comparación con los MA aislados de los pulmones, compartimiento afectado cuando la infección se vuelve sistémica entre el cuarto y sexto día de infección. La inmunidad contra T. gondii es similar entre ambas células fagocíticas, pero el tiempo de infección y el compartimiento donde se encuentren las células hace la diferencia en el tiempo de respuesta contra un parásito dado, en nuestro caso T. gondii. No hubo evidencia de que los sobrenadantes de cultivos de macrófagos provenientes de ratas infectadas ni el lisado de tripanosomas indujeran el efecto inmunosupresor.

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The immunosuppressive effect of Trypanosoma lewisi infection on alveolar macrophage (AM) activities against Cryptococcus neoformans was studied in an animal model. Two groups of rats were treated with T. lewisi and killed after 4 (4d-rats) and 7 days (7d-rats), respectively. A third group not given T. lewisi, served as control. AM were challenged in vitro with C. neoformans. Phagocytosis was assessed with a fluorescence method. Superoxide anion production was evaluated with the nitroblue tetrazolium (NBT) test. The survival of cryptococci was estimated by counting colony-forming units. The numbers of detached AM from culture plates were determined using a Bürker chamber. The NBT response, adhesion to plate surface and killing activity, but not the phagocytosis of AM from 4d-rats were significantly impaired compared to control or 7d-rats. Thus, T. lewisi causes transitory immunosuppressive effects on AM activities. This rapid T. lewisi immunosuppression model may be useful to study new approaches to anticryptococcal therapy.

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Peritoneal macrophages from Wistar rats, inoculated and non-inoculated with 10(6) T. lewisi trypomastigotes, were cultured and infected with 10(6) T. gondii tachyzoites. Multiplication rates of this parasite were studied after 1, 24 and 48 h of infection but there were not significant differences between the number of parasites found inside of macrophages coming, either from T. lewisi infected or non infected rats. On the other hand, in vivo studies of Toxoplasma multiplication inside peritoneal macrophages, showed that there is an increase of parasite number in cells from T. lewisi infected rats, as compared with those macrophages from non infected rats. This effect was statistically significant and was more evident after four days of infection. Therefore, it has been demonstrated that in vivo, but not in vitro T. lewisi infections, causes an important decrease of the natural resistance to T. gondii of the white rats, which is manifested by the major invasion and multiplication of the parasite inside of peritoneal macrophages.

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White rats were inoculated with 10(6) trypomastigotes of Trypanosoma lewisi, simultaneously or two days before and after inoculation with 10(5) oocysts of T. gondii. A greater number of cysts was found in the brain of the animals having concomitant inoculations, as compared with rats inoculated with either one of the two parasites. An apparent immunosuppressive effect is likely. Since both organisms can be found in rats, it is possible that infections with T. lewisi, could make this rodent another intermediate host for Toxoplasma infections.

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1. The immune responses to Trypanosoma cruzi infection of germfree mice were compared to the responses of infected conventional mice. Two groups (40 animals in each group) of 2-month old female CFW germfree and conventional mice were used. The IgM and IgG which bound to the surface of T. cruzi epimastigotes determined by ELISA were significantly lower in germfree than in conventional mice (1/3 and 1/5 for IgM and IgG, respectively). 2. After infection there was a three-fold increase in the circulating levels of these immunoglobulins in germfree but not in conventional mice. Twenty-one days after T. cruzi inoculation, both IgG and IgM levels were similar in germfree and conventional animals. 3. Footpad swelling after T. cruzi-antigen inoculation was initially four-fold more intense in germfree than in conventional mice. 4. These results suggest that the reduced humoral immune response of germfree mice during the initiation of experimental Chagas' disease may be responsible for the more severe parasitism when compared to conventional mice.

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1. The immune responses to Trypanosoma cruzi infection of germfree mice were compared to the reponses of infected conventional mice. Two groups (40 animals in each group) of 2-month old female CFW germfree and vonventional mice were used. The IgM and IgG which bound to the surface of T. cruzi epimastigotes determined by ELISA were significantly lower in germfree than in conventional mice (1/3 and 1/5 for IgM and IgG, respectively). 2. After infection there was a three-fold increase in the circulating levels of these immunoglobulins in germfree but not in conventional mice. twenty-one days after T. cruzi inoculation, both IgG and IgM levels were similar in germfree and conventional animals. 3. Footpad swelling after T. cruzi-antigen inoculation was initially four-fold more intense in germfree than in conventional mice. 4. These results suggest that the reduced humoral immune response of germfree mice during ythe initiation of experimental Chagas' disease may be responsible for the more severe parasitism when compared to conventional mice

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