Acanthamoeba isolates belonging to T1, T2, T3, T4 but not T7 encyst in response to increased osmolarity and cysts do not bind to human corneal epithelial cells

被引:42
作者
Dudley, R
Matin, A
Alsam, S
Sissons, J
Maghsood, AH
Khan, NA [1 ]
机构
[1] Univ London Birkbeck Coll, Sch Biol & Chem Sci, London WC1E 7HX, England
[2] Univ Tehran Med Sci, Dept Med Parasitol & Mycol, Sch Publ Hlth, Tehran 141556446, Iran
关键词
Acanthamoeba; cysts; encystment; osmolarity; adhesion;
D O I
10.1016/j.actatropica.2005.05.004
中图分类号
R38 [医学寄生虫学]; Q [生物科学];
学科分类号
07 ; 0710 ; 09 ; 100103 ;
摘要
Acanthamoeba is an opportunistic protozoan that is widely distributed in the environment and can cause human infections. The life cycle of Acanthamoeba consists of an infective trophozoite form. However under harsh environmental conditions trophozoites differentiate into a double-walled, metabolically inactive and resistant cyst form. Research in Acanthamoeba has mostly focussed on the infective trophozoite form and its pathogenic mechanisms. In this Study, we used Acanthamoeba isolates belonging to T1, T2, T3, T4, T7 genotypes and studied their cysts properties. We determined that food deprivation stimulates encystment in Acanthamoeba isolates belonging to T1, T2, T3, T4 and T7 genotypes in a sodium dodecyl sulfate (SDS)-resistant manner. In addition, increase in osmolarity triggered encystment in T1, T2, T3, T4 isolates (SDS-resistant) but T7 failed to encyst (SDS-labile). Adhesion assays revealed that Acanthamoeba cysts belonging to T1, T2, T3, T4, and T7 genotypes exhibited no and/or minimal binding (<5%) to the host cells. Fluorescein-labelled lectins showed that all Acanthamoeba isolates tested exhibited binding to concanavalin A, indicating the expression of mannosyl- and/or glucosyl-residues. Role of cysts in the transmission of infection is discussed further. (C) 2005 Elsevier B.V. All rights reserved.
引用
收藏
页码:100 / 108
页数:9
相关论文
共 28 条
[1]   Acanthamoeba interactions with human brain microvascular endothelial cells [J].
Alsam, S ;
Kim, KS ;
Stins, M ;
Rivas, AO ;
Sissons, J ;
Khan, NA .
MICROBIAL PATHOGENESIS, 2003, 35 (06) :235-241
[2]  
Araki-Sasaki K, 2000, J CELL PHYSIOL, V182, P189, DOI 10.1002/(SICI)1097-4652(200002)182:2<189::AID-JCP7>3.0.CO
[3]  
2-9
[4]  
Byers T.J., 1979, International Review of Cytology, V61, P283
[5]  
Cordingley JS, 1996, J CELL BIOCHEM, V61, P167
[6]   PUTATIVE VIRULENCE FACTORS OF CANDIDA-ALBICANS [J].
CUTLER, JE .
ANNUAL REVIEW OF MICROBIOLOGY, 1991, 45 :187-218
[7]  
FICKER L, 1990, Eye (London), V4, P835
[8]   Structure and expression of a cyst specific protein of Acanthamoeba castellanii [J].
Hirukawa, Y ;
Nakato, H ;
Izumi, S ;
Tsuruhara, T ;
Tomino, S .
BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION, 1998, 1398 (01) :47-56
[9]  
John David T., 1993, P143
[10]   Pathogenesis of Acanthamoeba infections [J].
Khan, NA .
MICROBIAL PATHOGENESIS, 2003, 34 (06) :277-285