Noradrenaline content of the hypothalamus and brain-stem of rats inoculated with Trypanosoma cruzi.
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Biomedical subjects
Publications and source records attributed to C R Machado.
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The injection of cercariae of Schistosoma mansoni into the peritoneal cavity of naive mice induces cell adhesion to these larvae, and this adherence sharply decreases when the infecting larva changes to schistosomule. This procedure was used to detect differences between schistosomules obtained in vivo and in vitro. Reinoculation of schistosomules obtained in vivo into the peritoneal cavity of mice did not trigger cell adhesion. In contrast, adherent cells were found in 4 and 24-hour-in vitro schistosomules. Our data on schistosomules obtained in vitro indicate that more than 24 hours are needed for complete remotion of molecules involved in the phenomenon of cell adhesion.
The peritoneal cavity of laboratory mice was used to study the phenomenon of host cell adhesion to different evolutive stages of the Schistosoma mansoni (cercaria, adult worm, developing and mature eggs, miracidium, young and mature daughter sporocysts). Material recovered from the peritoneal cavity 30 and 180 min after the inoculation of each evolutive form was examined with the help of a stereomicroscope. The free swimming larvae (cercaria and miracidium), and the evolutive forms producing such larvae (mature egg and mature daughter sporocyst) elicited the host cell adhesion phenomenon. In all forms but cercariae the adherent cells remained as so till 180 minutes after inoculation.
Cercariae of Schistosoma mansoni inoculated into the peritoneal cavity of naive mice induced host cell adhesion to their surface, but after 90 minutes the number of adherent cells sharply decreased. The cell detachment is progressive and simultaneous to the cercaria-schistosomule transformation. The histological study showed mainly neutrophils in close contact with the larvae. Mononuclear cells and some eosinophils were occasionally seen surrounding the adherent neutrophils. The scanning electron microscopy showed cells displaying twisted microvilli and several microplicae contacting or spreading over the larval surface, and larvae completely surrounded by clusters of cells. These results suggest that the neutrophils recognize molecules on the cercarial surface which induce their spreading.
Schistosoma mansoni cercariae were inoculated into the peritoneal cavity of naive mice and recovered 30 minutes later. Ultrastructural studies showed that neutrophils adhere to the larval surface and participate in the removal of glycocalyx by phagocytosis. This finding suggests that the neutrophils can play a role on the cercaria-schistosomulum transformation process.
Tissue parasitism, inflammatory process (histologic methods) and sympathetic denervation (glyoxylic acid-induced histofluorescence for demonstration of catecholamines) were studied in the heart (atrium and ventricle) and the submandibular gland of rats infected with the Y strain of Trypanosoma cruzi. In the heart paralleling intense parasitism and inflammatory process, the sympathetic denervation started at day-6 of infection and at the end of the acute phase (day 20) practically no varicose nerve terminals were found in both myocardium and vessels. In the submandibular gland, in spite of the rarity of amastigote pseudocysts and the scarcity of inflammatory foci, slight to moderate (days 13-15 of infection) or moderate to severe denervation (day 20) was found. At day 120 of infection both organs exhibited normal pattern of sympathetic innervation and only the heart showed some inflammatory foci and rare pseudocysts (ventricle). Our data suggest the involvement of circulating factors in the sympathetic denervation phenomena but indicate that local inflammatory process is, at least, an aggravating factor.
The parotid lymph nodes of naive and previously infected Balb/c mice were studied after, respectively, infection and re-infection with cercariae of Schistosoma mansoni via the ears. Schistosomula were able to pass through the lymph node by following the lymph flow or by penetrating the veins of the medullary cords. The number of nodal mast cells was higher from day 2 to 6 of primary infection; and from day 5 to 11 of re-infection. The amount of degranulating mast cells was significantly higher at day 4 of infection and at day 1 of re-infection. Eosinophils characterized the nodal inflammatory processes observed after day 5 in both primarily-infected and re-infected mice. However, only in the latter the eosinophils were able to adhere to the larval surface. In primarily-infected mice, no intranodal larva presented signs of degeneration. In contrast, in re-infected animals, some degenerating larvae were found inside eosinophilic infiltrates. The eosinophils reached the nodal tissue by migrating through the high endothelial venules and their collecting veins.
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