RESUMO
Observations by phase contrast, fluorescence and electron microscopy showed that epimastigotes of Trypanosoma (Schizotrypanum) dionisii (grown in vitro) were phagocytosed posterior end first by mouse peritoneal macrophages in vitro. Many were subsequently digested as a result of phagosome-lysosome fusion but others survived by apparently inhibiting this fusion and/or escaping from the phagosome into the host cell's cytoplasm. These survivors replicated as amastigotes. Long trypomastigotes, separated from populations grown in vitro by passage down a column of glass beads (with or without prior exposure to guinea-pig serum), were phagocytosed by either pole and all were subsequently digested.
Assuntos
Macrófagos/parasitologia , Trypanosoma/imunologia , Animais , Membrana Celular/ultraestrutura , Células Cultivadas , Lisossomos/ultraestrutura , Macrófagos/imunologia , Macrófagos/ultraestrutura , Camundongos , Microscopia Eletrônica , Microscopia de Fluorescência , Microscopia de Contraste de Fase , Fagocitose , Trypanosoma/ultraestruturaRESUMO
The attachment and entry of Trypanosoma dionisii to mouse peritoneal macrophages in vitro were studied. Both occurred to a similar extent whether parasites were alive or heat-killed, and whether macrophages were obtained from normal or immunized mice. Attachment occurred equally at 4 and 37 degrees C, but entry only occurred at the higher temperature. Neither was affected by pretreatment of parasites with active or inactivated complement. Entry, but not attachment, was inhibited by cytochalasin B; both were inhibited by trypsin. Immune mouse plasma (if inactivated) stimulated attachment but not entry (within 24 h). It also stimulated intracellular replication of T. dionisii by multiple fission and subsequent differentiation (probably within macrophages) to small extracellular trypomastigotes. No extracellular parasite and only scanty intracellular forms survived 120 h in cultures containing non-inactivated immune mouse plasma. It was concluded that attachment (in the absence of antibody) occurred to non-specific receptors in the macrophage membrane and was followed by phagocytosis of the parasites rather than their active penetration of the cell.
Assuntos
Macrófagos/fisiologia , Trypanosoma/fisiologia , Animais , Anticorpos , Células Cultivadas , Proteínas do Sistema Complemento , Citocalasina B/farmacologia , Macrófagos/efeitos dos fármacos , Camundongos , Morfogênese , Fagocitose/efeitos dos fármacos , Temperatura , Trypanosoma/crescimento & desenvolvimento , Tripsina/farmacologiaRESUMO
This paper explains the Canadian decision process following the isolation and identification of A/New Jersey/8/76 at Fort Dix, New Jersey in February 1976. The cause for concern was the emergence of a swine-like strain related to that which caused the 1918-19 pandemic, together with proved man-to-man transmission. This concern was reinforced since all new influenza A strains known to have infected the number of persons involved at Fort Dix have become strains of epidemic importance. The Fort Dix outbreak gave sufficient warning to allow implementation of a national vaccination program, to prevent and protect against influenza. In the past such an opportunity had not occurred, and vaccine use had, at best, constituted an intervention in the course of an outbreak. The National Advisory Committee on Immunizing Agents had all available information when it reached its decision to recommend vaccination with bivalent (A/Victoria and A/New Jersey) or with monovalent (A/New Jersey) vaccine for selective, high-risk groups. This was an independent, scientifically based decision.
