期刊
MICROBES AND INFECTION
卷 18, 期 1, 页码 57-67出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.micinf.2015.08.017
关键词
Cryptococcus; Monocytes; Brain endothelium; Phagocytosis; Transmigration
资金
- National Health and Medical Research Council of Australia [1050106]
- Rebecca L. Cooper Foundation
- Sydney Medical School Foundation
Cryptococcus neofonnans (Cn) and Cryptococcus gattii (Cg) cause neurological disease and cross the BBB as free cells or in mononuclear phagocytes via the Trojan horse mechanism, although evidence for the latter is indirect. There is emerging evidence that Cn and the North American outbreak Cg strain (R265) more commonly cause neurological and lung disease, respectively. We have employed a widely validated in vitro model of the BBB, which utilizes the hCMEC/D3 cell line derived from human brain endothelial cells (HBEC) and the human macrophage-like cell line, THP-1, to investigate whether transport of dual fluorescence-labelled Cn and Cg across the BBB occurs within macrophages. We showed that phagocytosis of Cn by non-interferon (IFN)-gamma stimulated THP-1 cells was higher than that of Cg. Although Cn and Cg-loaded THP-1 bound similarly to TNF-activated HBECs under shear stress, more Cn-loaded macrophages were transported across an intact HBEC monolayer, consistent with the predilection of Cn for CNS infection. Furthermore, Cn exhibited a higher rate of expulsion from transmigrated THP-1 compared with Cg. Our results therefore provide further evidence for transmigration of both Cn and Cg via the Trojan horse mechanism and a potential explanation for the predilection of Cn to cause CNS infection. (C) 2015 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.
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