Experimental infection of murine splenic lymphocytes and granulocytes with Toxoplasma gondii RH tachyzoites
Author(s) -
J Y Chai,
J Kook,
Sang-Mee Guk,
Yuan Chang,
C K Yun
Publication year - 1997
Publication title -
korean journal of parasitology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.555
H-Index - 42
eISSN - 1738-0006
pISSN - 0023-4001
DOI - 10.3347/kjp.1997.35.2.79
Subject(s) - toxoplasma gondii , biology , intracellular parasite , vacuole , intracellular , immune system , cytoplasm , parasite hosting , spleen , microbiology and biotechnology , ultrastructure , virology , immunology , antibody , anatomy , world wide web , computer science
Toxoplasma gondii, an intracellular protozoan infecting many kinds of eukaryotic cells, has been used to experimentally infect macrophages, epithelial cells, fibroblasts, and various cancer cells, but rarely T and B lymphocytes or granulocytes. The present study was performed to determine the susceptibility of murine (BALB/c or CBA) splenic T and B lymphocytes, and granulocytes to infection with T. gondii RH tachyzoites. The ultrastructure of the infected host cells was observed by TEM, and the degree of intracellular parasite proliferation was quantified using 3H-uracil uptake assay. At 24 hrs post-culture, the host cell cytoplasm was found to contain 1 or 2, or a maximum of 7-8 tachyzoites. Infected T lymphocytes demonstrated a peripherally displaced nucleus, a parasitophorous vacuole enveloping the parasite, and an increased number of mitochondria. In B lymphocytes infected with tachyzoites, RER was not well developed compared to uninfected B lymphocytes. Uninfected granulocytes contained many electron-dense granules, but T. gondii-infected granulocytes demonstrated a decreased number of granules. Based on the 3H-uracil uptake assay, the susceptibility of T and B lymphocytes, and granulocytes, to infection with T. gondii tachyzoites was fairly high irrespective of cell type and strain of mouse. This strongly suggests deterioration in the functioning of infected host immune cells.
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