Porcine Small Intestinal Epithelial Cell Line (IPEC-J2) of Rotavirus Infection As a New Model for the Study of Innate Immune Responses to Rotaviruses and Probiotics
Porcine Small Intestinal Epithelial Cell Line (IPEC-J2) of Rotavirus Infection As a New Model for the Study of Innate Immune Responses to Rotaviruses and Probiotics
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DOI：
10.1089/vim.2009.0088
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发表时间：
2010-04-01
期刊：
影响因子：
2.2
通讯作者：
Yuan, Lijuan
中科院分区：
文献类型：
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作者：
Liu, Fangning;Li, Guohua;Yuan, Lijuan
以前的研究上皮细胞对轮状病毒感染的免疫反应已经在转化细胞系中进行。在这项研究中，我们评估了非转化猪空肠上皮细胞系（IPEC-J2）作为轮状病毒感染和益生菌治疗的体外模型。将细胞培养适应的猪轮状病毒（PRV）OSU株或人轮状病毒（HRV）Wa株与嗜酸乳杆菌（LA）或鼠李糖乳杆菌GG（LGG）一起沿着用于培养IPEC-J2细胞。在轮状病毒感染前或感染后应用LA或LGG治疗。我们证明了IPEC-J2细胞被PRV高效感染。LA或LGG处理细胞不会减少病毒复制。PRV感染增加MUC 3粘蛋白分泌。轮状病毒感染后LGG处理减少了PRV诱导的粘蛋白分泌反应;单独LGG增加了膜相关MUC 3粘蛋白的产生。在轮状病毒感染之前，LA治疗显著增加PRV复制和对PRV感染的IL-6应答，这与LA的佐剂作用一致。轮状病毒感染后LGG治疗下调了IL-6反应，证实了LGG的抗炎作用。IPEC-J2细胞组成型表达Toll样受体（TLR）2、TLR 3和TLR 9。TLR 2的表达上调LGG和肽聚糖，对应于降低的IL-6反应，表明LGG的保护作用与TLR 2表达上调肠上皮细胞。PRV感染的IPEC-J2细胞模型是一个完全同源的系统。该模型为研究轮状病毒-宿主-益生菌之间的相互作用以及益生菌对先天免疫应答的免疫调节作用机制提供了一个有价值的模型。
Previous studies of epithelial immune responses to rotavirus infection have been conducted in transformed cell lines. In this study, we evaluated a non-transformed porcine jejunum epithelial cell line (IPEC-J2) as an in-vitro model of rotavirus infection and probiotic treatment. Cell-culture-adapted porcine rotavirus (PRV) OSU strain, or human rotavirus (HRV) Wa strain, along with Lactobacillus acidophilus (LA) or Lactobacillus rhamnosus GG (LGG) were used to inoculate IPEC-J2 cells. LA or LGG treatment was applied pre-or post-rotavirus infection. We demonstrated that IPEC-J2 cells were productively infected by PRV. LA or LGG treatment of the cells did not reduce virus replication. PRV infection increased MUC3 mucin secretion. LGG treatment post-rotavirus infection reduced the mucin secretion response induced by PRV; LGG alone increased the production of membrane-associated MUC3 mucin. LA treatment prior to rotavirus infection significantly increased PRV replication and the IL-6 response to PRV infection, which is consistent with the adjuvant effect of LA. LGG treatment post-rotavirus infection downregulated the IL-6 response, confirming the anti-inflammatory effect of LGG. IPEC-J2 cells expressed toll-like receptor (TLR) 2, TLR3, and TLR9 constitutively. TLR2 expression was upregulated by LGG and peptidoglycan, corresponding to the decreased IL-6 response, indicating that the protective effect of LGG is associated with upregulation of TLR2 expression on intestinal epithelial cells. The IPEC-J2 cell model of PRV infection is a completely homologous system. It is a valuable model for studying the interactions among rotavirus-host-probiotics, and the mechanisms behind the immunomodulating effect of probiotic bacteria on innate immune responses.