TY - JOUR
T1 - Acanthamoeba interactions with human brain microvascular endothelial cells
AU - Alsam, Selwa
AU - Kim, Kwang Sik
AU - Stins, Monique
AU - Rivas, Antonio Ortega
AU - Sissons, James
AU - Khan, Naveed Ahmed
N1 - Funding Information:
The author is grateful to Drs Greg Booton and Thomas Byers (The Ohio State University) for providing genotypes of Acanthamoeba quina and A. divionensis . This work was supported by grants from Faculty Research Fund, Central Research Fund, University of London and The Royal Society.
PY - 2003/12
Y1 - 2003/12
N2 - Acanthamoeba are opportunistic protozoan parasites that can cause fatal granulomatous amoebic encephalitis, however, the pathogenic mechanisms associated with this disease remain unclear. One of the primary factors in Acanthamoeba encephalitis is the haematogenous spread, followed by invasion of the blood-brain barrier resulting in the transmigration of Acanthamoeba into the central nervous system. In this study, we have used human brain microvascular endothelial cells, which constitute the blood-brain barrier and studied their interactions with Acanthamoeba. Using in vitro cultures, we showed that Acanthamoeba isolates belonging to genotypes T3, T4 and T11, exhibited increased cytotoxicity on human brain microvascular endothelial cells as well as exhibited higher binding and were considered potential pathogens. In contrast, Acanthamoeba isolates belonging to genotypes T2 and T7 exhibited minimal cytotoxicity and significantly less binding to human brain microvascular endothelial cells (P<0.01). Furthermore, exogenous α-mannose inhibited binding but increased cytotoxicity of human brain microvascular endothelial cells. This is the first demonstration of Acanthamoeba interactions with primary human brain microvascular endothelial cells.
AB - Acanthamoeba are opportunistic protozoan parasites that can cause fatal granulomatous amoebic encephalitis, however, the pathogenic mechanisms associated with this disease remain unclear. One of the primary factors in Acanthamoeba encephalitis is the haematogenous spread, followed by invasion of the blood-brain barrier resulting in the transmigration of Acanthamoeba into the central nervous system. In this study, we have used human brain microvascular endothelial cells, which constitute the blood-brain barrier and studied their interactions with Acanthamoeba. Using in vitro cultures, we showed that Acanthamoeba isolates belonging to genotypes T3, T4 and T11, exhibited increased cytotoxicity on human brain microvascular endothelial cells as well as exhibited higher binding and were considered potential pathogens. In contrast, Acanthamoeba isolates belonging to genotypes T2 and T7 exhibited minimal cytotoxicity and significantly less binding to human brain microvascular endothelial cells (P<0.01). Furthermore, exogenous α-mannose inhibited binding but increased cytotoxicity of human brain microvascular endothelial cells. This is the first demonstration of Acanthamoeba interactions with primary human brain microvascular endothelial cells.
KW - Acanthamoeba
KW - Adhesion
KW - Cytotoxicity
KW - Granulomatous amoebic encephalitis
KW - Mannose-binding protein
KW - Pathogenic protozoa
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U2 - 10.1016/j.micpath.2003.07.001
DO - 10.1016/j.micpath.2003.07.001
M3 - Article
C2 - 14580387
AN - SCOPUS:0242289618
SN - 0882-4010
VL - 35
SP - 235
EP - 241
JO - Microbial Pathogenesis
JF - Microbial Pathogenesis
IS - 6
ER -