Rotavirus infection induces an increase in intracellular calcium concentration in human intestinal epithelial cells:: Role in microvillar actin alteration
Rotavirus infection induces an increase in intracellular calcium concentration in human intestinal epithelial cells:: Role in microvillar actin alteration
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DOI：
10.1128/jvi.74.5.2323-2332.2000
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发表时间：
2000-03-01
影响因子：
5.4
通讯作者：
Servin, A
中科院分区：
文献类型：
--
作者：
Brunet, JP;Cotte-Laffitte, J;Servin, A
Rotaviruses, which infect mature enterocytes of the small intestine, are recognized as the most important cause of viral gastroenteritis in young children. We have previously reported that rotavirus infection induces microvillar F-actin disassembly in human intestinal epithelial Caco-2 cells (N, Jourdan, J, P, Brunet, C, Sapin, A, Blais, J, Cotte Laffitte, F, Forestier, A, M, Quero, G. Trugnant and A, L, Servin, J, Virol, 72:7228-7236, 1998), In this study, to determine the mechanism responsible for rotavirus-induced F-actin alteration, we investigated the effect of infection on intracellular calcium concentration ([Ca2+](i)) in Caco-2 cells, since Ca2+ is known to be a determinant factor for actin cytoskeleton regulation. As measured by quin2 fluorescence, viral replication induced a progressive increase in [Ca2+](i) from 7 h postinfection, which was shown to be necessary and sufficient for microvillar F-actin disassembly, During the first hours of infection, the increase in [Ca2+](i) was related only to an increase in Ca2+ permeability of plasmalemma, At a late stage of infection, [Ca2+](i) elevation was due to both extracellular Ca2+ influx and Ca2+ release from the intracellular organelles, mainly the endoplasmic reticulum (ER), We noted that at this time the [Ca2+](i) increase was partially related to a phospholipase C (PLC)-dependent mechanism, which probably explains the Ca2+ release from the ER, We also demonstrated for the first time that viral proteins or peptides, released into culture supernatants of rotavirus-infected Caco-2 cells, induced a transient increase in [Ca2+](i) of uninfected Caco-2 cells, by a PLC dependent efflux of Ca2+ from the ER and by extracellular Ca2+ influx. These supernatants induced a Ca2+-dependent microvillar F-actin alteration in uninfected Caco-2 cells, thus participating in rotavirus pathogenesis.
