Glomerular changes and alterations of zonula occludens-1 in the kidneys of Plasmodium falciparum malaria patients

Malaria Journal

Research

Urai Chaisri¹  Parnpen Viriyavejakul¹  Benjamas Wichapoon¹  Chuchard Punsawad² 

[1] Department of Tropical Pathology, Faculty of Tropical Medicine, Mahidol University, 420/6 Rajvithi Road, 10400, Bangkok, Thailand;School of Medicine, Walailak University, 222 Thasala District, 80161, Nakhon Si Thammarat, Thailand;

关键词: Zonula occludens-1;    ZO-1;    Tight junction;    Kidney;    Glomeruli;    Plasmodium falciparum;    Acute kidney injury;    AKI;   

DOI  :  10.1186/1475-2875-13-176

 received in 2014-01-24, accepted in 2014-04-29,  发布年份 2014

来源: Springer

【 摘 要 】

BackgroundThe process of cytoadhesion in Plasmodium falciparum malaria infection causes signaling processes that lead to structural and functional changes at the cellular level. Histopathological changes of acute kidney injury (AKI) in P. falciparum malaria often involve glomerular proliferation, thickening of the glomerular basement membrane, acute tubular necrosis, and interstitial inflammation. Focusing on the glomeruli, this study aimed to investigate glomerular and tight junction-associated protein- zonula occludens-1 (ZO-1) changes in P. falciparum malaria patients.MethodsKidney tissues were grouped into P. falciparum with AKI (Cr ≥ 265 μmol/L or 3 mg/dl), P. falciparum without AKI (Cr < 265 μmol/L), and normal kidney tissues (control group). Glomerular cells and the glomerular area were quantified and compared in three experimental groups. The tight junction was investigated immunohistochemically using tight junction-associated protein, ZO-1, protein marker. A further immunofluorescence study was performed in an endothelial cell (EC)-parasitized red blood cell (PRBC) co-culture system, to evaluate the tight junction protein.ResultsGlomerular cell proliferation was significant in P. falciparum with AKI (Cr ≥ 265 μmol/L). By contrast, the glomerular area decreased significantly. ZO-1 expression was significantly decreased in the AKI group compared with normal kidneys, and in kidney tissues without AKI (p < 0.05). This was further confirmed by the depletion in ZO-1 localization in ECs co-cultured with PRBCs.ConclusionsIn P. falciparum malaria with AKI, the decrease in glomerular area, despite glomerular cell proliferation, could be due to the collapse of cellular structures secondary to damaged tight junction-associated protein, ZO-1.

【 授权许可】

Unknown   
© Wichapoon et al.; licensee BioMed Central Ltd. 2014. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.