Differential effects of Sendai virus infection on mediator synthesis by mesangial cells from two mouse strains.
Differential effects of Sendai virus infection on mediator synthesis by mesangial cells from two mouse strains.
复制标题
仙台病毒感染对两种小鼠品系系膜细胞介质合成的不同影响。
DOI：
10.1046/j.1523-1755.2003.00258.x
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发表时间：
2003
期刊：
影响因子：
--
通讯作者：
Emancipator,StevenN
中科院分区：
文献类型：
--
作者：
Kobayashi,Noriyoshi;Bagheri,Nayer;Nedrud,JohnG;Strieter,RobertM;Tomino,Yasuhiko;Lamm,MichaelE;Emancipator,StevenN
Differential effects of Sendai virus infection on mediator synthesis by mesangial cells from two mouse strains.BackgroundRecently, we observed that the severity of glomerulonephritis in an experimental model of immunoglobulin A nephropathy (IgAN) induced by Sendai virus differs between C57BL/6 and BALB/c mouse strains. The determinants of differing renal insufficiency are not understood. In the present study, we examine the capacity for mesangial cells to support Sendai viral replication and assess the direct effects of Sendai virus on the production of selected cytokines, chemokines, and eicosanoids by mesangial cells, comparing C57BL/6 to BALB/c mouse strains.MethodsSendai virus replication was measured by viral plaque assay using LLCMK2 cells. Production of cytokines [interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α)], chemokines (JE and KC), and eicosanoids [prostaglandin E2(PGE2) and thromboxane B2(TxB2)] in culture medium was evaluated by sandwich enzyme-linked immunosorbent assay (ELISA) or competitive enzyme immunoassay (EIA) after 48 hours' incubation with infectious or inactivated Sendai virus.ResultsSendai virus replicates equally well in mesangial cells from both strains, and infection evokes increased IL-6, JE, KC, and PGE2production in relation to viral dose. BALB/c mesangial cells produce significantly more IL-6 and JE than those from C57BL/6, and the dose response for KC is steeper in BALB/c mesangial cells than those from C57BL/6. Synthesis of PGE2in BALB/c mesangial cells is higher than that of C57BL/6 mesangial cells, both under basal conditions and in response to infectious Sendai virus, again in a dose-dependent manner. There is no TNF-α or thromboxane response to viral stimulation.ConclusionWe conclude that different mesangial cell responses to this common mucosal viral pathogen might influence the severity of IgAN in our model system.
