原创力文档sialoglycosylation of rbc in visceral leishmaniasis leads to enhanced oxidative stress, calpain-induced fragmentation of spectrin and hemolysissialoglycosylation红细胞的内脏利什曼病导致增强氧化应激,calpain-induced碎片的血影蛋白和溶血.pdfVIP
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sialoglycosylation of rbc in visceral leishmaniasis leads to enhanced oxidative stress, calpain-induced fragmentation of spectrin and hemolysissialoglycosylation红细胞的内脏利什曼病导致增强氧化应激,calpain-induced碎片的血影蛋白和溶血
Sialoglycosylation of RBC in Visceral Leishmaniasis Leads
to Enhanced Oxidative Stress, Calpain-Induced
Fragmentation of Spectrin and Hemolysis
1 1¤ 1 2 3
Sajal Samanta , Angana Ghoshal , Kaushik Bhattacharya , Bibhuti Saha , Peter Walden ,
Chitra Mandal1*
1 Cancer Biology and Inflammatory Disorder Division; CSIR-Indian Institute of Chemical Biology, Kolkata, India, 2 Department of Tropical Medicine, School of Tropical
´ ¨
Medicine, Kolkata, India, 3 Department of Dermatology, Charite-Universitatsmedizin Berlin, Humboldt University Berlin, Germany
Abstract
Visceral leishmaniasis (VL) caused by the intracellular parasite Leishmania donovani accounts for an estimated 12 million
cases of human infection. It is almost always associated with anemia, which severely complicates the disease course.
However, the pathological processes leading to anemia in VL have thus far not been adequately characterized to date. In
studying the glycosylation patterns of peripheral blood cells we found that the red blood cells (RBC) of VL patients (RBCVL)
express eight 9-O-acetylated sialoglycoproteins (9-O-AcSGPs) that are not detected in the RBC of healthy individuals (RBCN).
At the same time, the patients had high titers of anti-9-O-AcSGP IgG antibodies in their sera. These two conditions appear to
be linked and related to the anemic state of the patients, as exposure of RBCVL but not RBCN to anti-9-O-AcSGPs antibodies
purified from patient sera triggered a series of responses. These included calcium influx via the P/Q-type but not L-type
channels, activation of calpain I, proteolysis of spectrin, enhanced oxidative stress, lipid peroxidation, external
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