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1.
The Korean Journal of Parasitology ; : 185-193, 2004.
Article in English | WPRIM | ID: wpr-177059

ABSTRACT

Toxoplasma gondii is an obligate intracellular protozoan parasite, which invades a wide range of hosts including humans. The exact mechanisms involved in its invasion are not fully understood. This study focused on the roles of Ca2+ in host cell invasion and in T. gondii replication. We examined the invasion and replication of T. gondii pretreated with several calcium modulators, the conoid extrusion of tachyzoites. Calmodulin localization in T. gondii were observed using the immunogold method, and Ca2+ levels in tachyzoites by confocal microscopy. In light microscopic observation, tachyzoites co-treated with A23187 and EGTA showed that host cell invasion and intracellular replication were decreased. The invasion of tachyzoites was slightly inhibited by the Ca2+ channel blockers, bepridil and verapamil, and by the calmodulin antagonist, calmidazolium. We observed that calcium saline containing A23187 induced the extrusion of tachyzoite conoid. By immunoelectron microscopy, gold particles bound to anti-calmodulin or anti-actin mAb, were found to be localized on the anterior portion of tachyzoites. Remarkably reduced intracellular Ca2+ was observed in tachyzoites treated with BAPTA/AM by confocal microscopy. These results suggest that host cell invasion and the intracellular replication of T. gondii tachyzoites are inhibited by the calcium ionophore, A23187, and by the extracellular calcium chelator, EGTA.


Subject(s)
Animals , Humans , Calcium/physiology , Calcium Channel Blockers/pharmacology , Calmodulin/antagonists & inhibitors , Chelating Agents/pharmacology , HeLa Cells , Host-Parasite Interactions , Ionophores/pharmacology , Toxoplasma/drug effects
2.
Microbiology ; (12)1992.
Article in Chinese | WPRIM | ID: wpr-685701

ABSTRACT

Brucella organisms are facultative intracellular bacteria capable of surviving inside professional and non-professional phagocytes.Upon cell contact the bacteria is internalized via receptor molecules.Once inside cells,Brucella localizes in early phagosomes,where it avoids fusion with late endosomes and lysosomes.Then,the bacterium redirects its trafficking to autophagosomes and finally reaches the endoplasmic reticulum,the replicating niche.Once inside the endoplasmic reticulum,Brucella extensively replicates without restricting basic cellular functions or inducing damage to cells.Invasion,intracellular trafficking and replication of Brucella organisms in professional and non-professional phagocytes and the molecular determinants involving Brucella intracellular life are reviewed in this article.

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