Publication: Glomerular changes and alterations of zonula occludens-1 in the kidneys of Plasmodium falciparum malaria patients.
1
Accepted Date
2014-04-29
Issued Date
2014-05-09
Copyright Date
2014
Resource Type
Language
eng
ISSN
1475-2875 (electronic)
Rights
Mahidol University
Rights Holder(s)
BioMed Central
Bibliographic Citation
Wichapoon B, Punsawad C, Chaisri U, Viriyavejakul P. Glomerular changes andalterations of zonula occludens-1 in the kidneys of Plasmodium falciparum malaria patients. Malar J. 2014 May 9;13:176.
Suggested Citation
Benjamas Wichapoon, เบญจมาศ วิชาพูล, Chuchard Punsawad, ชูชาติ พันธ์สวัสดิ์, Urai Chaisri, อุไร ไชยศรี, Parnpen Viriyavejakul, พรรณเพ็ญ วิริยเวชกุล Glomerular changes and alterations of zonula occludens-1 in the kidneys of Plasmodium falciparum malaria patients.. Wichapoon B, Punsawad C, Chaisri U, Viriyavejakul P. Glomerular changes andalterations of zonula occludens-1 in the kidneys of Plasmodium falciparum malaria patients. Malar J. 2014 May 9;13:176.. doi:10.1186/1475-2875-13-176. Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/780
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Title
Glomerular changes and alterations of zonula occludens-1 in the kidneys of Plasmodium falciparum malaria patients.
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Abstract
BACKGROUND: The 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.
METHODS: Kidney 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.
RESULTS: Glomerular 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.
CONCLUSIONS: In 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.