In mice infected with virulent blood (trypomastigote) forms of Trypanosoma cruzi, complement depletion with cobra venom factor caused a marked exacerbation of the disease evidenced by significantly increased parasitemia levels and early mortality as compared with those of untreated infected animals. The effect was greater in mice receiving cobra venom factor on day 7 postinfection, i.e., at the time when the parasites had had time to localize and multiply in the tissues and appeared in the circulation in appreciable numbers. The possibility that complement participates in host defense against T. cruzi infection through a mechanism involving immune lysis was explored in vitro. T. cruzi trypomastigotes were found to undergo immune lysis in sera of patients with chronic Chagas' disease, in sera of immunized mice, and in solutions containing both immune mouse gamma globulin and a source of active complement. This phenomenon failed to take place either in the absence of complement or after complement inactivation by heat or utilizing complement inactivators. The lytic capacity of heated sera was restored by the addition of active complement to the system. During the immune lysis of T. cruzi blood forms, complement was activated in human sera via both the classical and the alternate pathways. In mouse sera, activation followed at least the alternate pathway.
This is the first report objectively suggesting (by means of rPAS) a correlation between the brain neuroplastic changes induced by Vitalstim and the swallowing function improvement. It is hypothesizable that Vitalstim may have targeted cortical (and maybe subcortical) brain areas that are recruited during the highly coordinated function of swallowing, and it may have thus potentiated the well-known neuroplastic changes induced by repetitive and intensive swallowing exercises, probably thanks to metaplasticity phenomena.
In mice, depression of reticuloendothelial activity by intravenous injection of silica particles resulted in a decreased resistance to infection with virulent blood forms (trypomastigotes) of Trypanosoma cruzi. In these animals, both the mortality rate and the levels of parasitemia were significantly increased over those of control mice given only the parasites. Accordingly, stimulation of the reticuloendothelial system (RES) with diethylstilbestrol (DES) before infection reduced considerably both the mortality rate and the levels of parasitemia, and prolonged the survival time after infection. Although in low percentages (16 to 25%), survival after the 60-day observation period was observed only among mice which had been treated with DES.
Virulent trypomastigote forms of T. cruzi were found inside mouse peritoneal macrophages shortly after intraperitoneal (i.p.) injection. Many of the parasites were killed within these cells both in vivo and in vitro.
The data reported in this paper indicate that, in the mouse, the RES is involved in the resistance against infection with virulent blood forms of T. cruzi, possibly through the capacity of macrophages to destroy the parasite.
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