Secretory organelles of pathogenic protozoa

Processos de secreção celular desempenham papel relevante na biologia e no ciclo de vida de protozoários patogênicos. A presente revisão analisa, sob uma perspectiva de biologia celular, o processo de secreção em (a) micronemas, roptrias e grânulos densos encontrados em membros do grupo Apicomplexa, onde essas estruturas participam da penetração do protozoário no interior da célula hospedeira, na sua sobrevivência intravacuolar e no posterior egresso da célula hospedeira, (b) a fenda de Maurer, encontrada em Plasmodium, uma estrutura envolvida na secreção de proteínas sintetizadas pelo protozoário intravacuolar e transportada, através de vesículas, para a superfície do eritrócito, (c) a secreção de macromoléculas na bolsa flagelar de tripanosomatídeos, e (d) a secreção de proteínas que fazem parte da parede cística de Giardia e Entamoeba e que se concentram nas vesículas de encistamento.

Behaviour of microtubules in cells infected with Toxoplasma gondii

Toxoplasma gondii proliferates within the parasitophorous vacuole of the host cell. Simultaneously with parasite division and vacuolar development, lipids traffic and change in the spatial distribution of organelles of the host cell cytoplasm occur. Using fluorescence microscopy, and antibodies recognizing tubulin, we showed that microtubules change their distribution during host cell infection by tachyzoites of T. gondii. In addition, transmission electron microscopy of thin sections and replicas of partially extracted cells showed that host cell microtubules concentrate around the parasitophorous vacuole. Such microtubules distribution was evident in early infection times and was more prominent after 24 h of infection, when parasitophorous vacuole was completely surrounded by microtubules. However, the meshwork microtubule filaments became slack or absent after 72 h of infection of host cell. Colchicine and taxol treatment altered the shape of the parasitophorous vacuole containing tachyzoites. These observations suggest a close association between microtubules and intravacuolar development of parasites.

Role of the microtubular system in platelet aggregation

1. Four structural systems are involved in the process of platelet activation that leads to aggregation: 1) the membrane system, i.e., the cytoplasmic membrane, the dense tubular structure and the open canalicular structure; 2) alpha and dense granules; 3) the peripheral microtubular coils; 4) the microfibrillar meshwork of actin-myosin bundles. 2. We added four compounds which modify cell ultrastructure to normal platelet-rich plasma to analyze the behavior of the structural systems of platelet activation: vinblastine (100 micrograms/ml) and cimetidine (100 micrograms/ml) that act on the membrane system, ticlopidine (200 micrograms/ml) and colchicine (100 micrograms/ml) that affect primarily the microtubular structure, cytochalasin B (30 micrograms/ml) and phorbol myristate acetate (100 ng/ml) that act upon the granular system, and cytochalasin D (30 micrograms/ml) and concanavalin A (50 micrograms/ml) that influence the microfibrillar structure. Platelet aggregation was stimulated by epinephrine or thrombin. 3. Cimetidine and ticlopidine prevented aggregation. However, neither substance affected the microtubular structure. Colchicine and cytochalasin B only partially impaired aggregation, because pieces of microtubules remained in the presence of these substances. The other substances did not present anti-aggregant activity and did not preserve the microtubules. 4. We infer that the disappearance of the microtubules is necessary to produce aggregation. When they remain intact no aggregation is produced, even though the other structural systems are activated.