Involvement of lectin pathway activation in the complement killing of Giardia intestinalis

被引:34
作者
Evans-Osses, Ingrid [1 ,2 ]
Ansa-Addo, Ephraim A. [3 ]
Inal, Jameel M. [3 ]
Ramirez, Marcel I. [1 ]
机构
[1] Fiocruz MS, Inst Oswaldo Cruz, Lab Biol Mol Parasitas & Vetores, BR-21040900 Rio De Janeiro, Brazil
[2] Fiocruz MS, Inst Oswaldo Cruz, Lab Interdisciplinar Pesquisas Med LIP Med, BR-21040900 Rio De Janeiro, Brazil
[3] London Metropolitan Univ, Fac Life Sci, Cellular & Mol Immunol Res Ctr, London N7 8DB, England
关键词
Giardia intestinalis; Lectin pathway; Trophozoites; Complement-mediated killing; Intestinal disease; Mannose; GlcNAc; CELL-DEPENDENT CONTROL; LAMBLIA TROPHOZOITES; LINKED GLYCANS; INFECTIONS;
D O I
10.1016/j.bbrc.2010.04.025
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Giardia intestinalis (syn. G. lamblia, G. duodenalis) is a flagellated unicellular eukaryotic microorganism that commonly causes diarrheal disease throughout the world. In humans, the clinical effects of Giardia infection range from the asymptomatic carrier state to a severe malabsorption syndrome possibly due to different virulence of the Giardia strain, the number of cysts ingested, the age of the host, and the state of the host immune system at the time of infection. The question about how G. intestinalis is controlled by the organism remains unanswered. Here, we investigated the role of the complement system and in particular, the lectin pathway during Giardia infections. We present the first evidence that G. intestinalis activate the complement lectin pathway and in doing so participate in eradication of the parasite. We detected rapid binding of mannan-binding lectin, H-ficolin and L-ficolin to the surface of G. intestinalis trophozoites and normal human serum depleted of these molecules failed to kill the parasites. Our finding provides insight into the role of lectin pathway in the control of G. intestinalis and about the nature of surface components of parasite. (C) 2010 Elsevier Inc. All rights reserved.
引用
收藏
页码:382 / 386
页数:5
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