Regulation role of ADAM17 on porcine reproductive and respiratory syndrome virus infection
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- 英文论文题名：Regulation role of ADAM17 on porcine reproductive and respiratory syndrome virus infection
- 论文作者：Yue Wang ; Guo longjun ; Li Ren ; Gu Weihong
- 英文论文作者：Yue Wang ; Guo longjun ; Li Ren ; Gu Weihong ; Harbin Veterinary Research Institute ; Chinese Academy of Agricultural Sciences
- 年：2016
- 作者机构：Harbin Veterinary Research Institute,Chinese Academy of Agricultural Sciences;
- 英文论文关键词：PRRSV ; ADAM17 ; ectodomain shedding ; TNFa ; CD16
- 会议召开时间：2016-11-04
- 会议录名称：第十一届全国免疫学学术大会摘要汇编
- 英文会议录名称：Abstracts of 2016 CSI Congress on Immunology
- 语种：英文
- 分类号：S852.651
- 学会代码：IGMD
- 会议名称：第十一届全国免疫学学术大会
- 会议地点：中国安徽合肥
- 主办单位：中国免疫学会
- 学会名称：中国免疫学会
- 页数：1
- 文件大小：975k
- 原文格式：D
- 会议级别：全国
摘要
Aim: Metalloprotease ADAM17 has been implicated in the control of cancer, inflammation, and other pathologies. However, the role of ADAM17 on virus infection has been rarely studied. In this study, we are investigated the regulation role of metalloprotease ADAM17 on porcine reproductive and respiratory virus(PRRSV) infection. Methods: The activity of ADAM17 has been modified by siRNA, inhibitor, overexpression, and stimulator, the role of ADAM17 on TNFa secretion, virus replication, receptor expression, has been examined by using flow cytometry, ELISA, Western-blot, confocal, and TCID50. Results: First, we found that porcine alveolar macrophages produced a great amount of soluble TNFα upon PRRSV infection, and this soluble TNFα in turn has great anti-PRRSV effect. By using inhibitor and genetic modification methods, we addressed that the production of porcine TNFα was mediated by ADAM17. Next, we found that inhibition of ADAM17 activity facilitated PRRSV infection in different target cells. Furthermore, we revealed that virus infection-activated ADAM17 can cleave PRRSV receptor CD163, which thus hinders virus entry. Lastly, we discovered that PRRSV treatment also can stimulate porcine neutrophils to produce soluble form of CD16(s CD16) in vivo and in vitro, which can serve as a biomarker for PRRSV infection. We then proved that the production of s CD16 is also an ADAM17-mediated ectodomain shedding event. Since we have shown that CD16 is involved in antibody-dependent enhancement(ADE) of PRRSV, this result indicates that the downregulation of CD16 might restrict CD16-mediated ADE effect of PRRS. Conclusion: PRRSV infection can stimulate ADAM17, which subsequently plays an anti-virus role through cleaving its substrates. Our findings suggest that activation of ADAM17 may be useful in enhancing the porcine anti-PRRSV response.
Aim: Metalloprotease ADAM17 has been implicated in the control of cancer, inflammation, and other pathologies. However, the role of ADAM17 on virus infection has been rarely studied. In this study, we are investigated the regulation role of metalloprotease ADAM17 on porcine reproductive and respiratory virus(PRRSV) infection. Methods: The activity of ADAM17 has been modified by siRNA, inhibitor, overexpression, and stimulator, the role of ADAM17 on TNFa secretion, virus replication, receptor expression, has been examined by using flow cytometry, ELISA, Western-blot, confocal, and TCID50. Results: First, we found that porcine alveolar macrophages produced a great amount of soluble TNFα upon PRRSV infection, and this soluble TNFα in turn has great anti-PRRSV effect. By using inhibitor and genetic modification methods, we addressed that the production of porcine TNFα was mediated by ADAM17. Next, we found that inhibition of ADAM17 activity facilitated PRRSV infection in different target cells. Furthermore, we revealed that virus infection-activated ADAM17 can cleave PRRSV receptor CD163, which thus hinders virus entry. Lastly, we discovered that PRRSV treatment also can stimulate porcine neutrophils to produce soluble form of CD16(s CD16) in vivo and in vitro, which can serve as a biomarker for PRRSV infection. We then proved that the production of s CD16 is also an ADAM17-mediated ectodomain shedding event. Since we have shown that CD16 is involved in antibody-dependent enhancement(ADE) of PRRSV, this result indicates that the downregulation of CD16 might restrict CD16-mediated ADE effect of PRRS. Conclusion: PRRSV infection can stimulate ADAM17, which subsequently plays an anti-virus role through cleaving its substrates. Our findings suggest that activation of ADAM17 may be useful in enhancing the porcine anti-PRRSV response.
Aim: Metalloprotease ADAM17 has been implicated in the control of cancer, inflammation, and other pathologies. However, the role of ADAM17 on virus infection has been rarely studied. In this study, we are investigated the regulation role of metalloprotease ADAM17 on porcine reproductive and respiratory virus(PRRSV) infection. Methods: The activity of ADAM17 has been modified by siRNA, inhibitor, overexpression, and stimulator, the role of ADAM17 on TNFa secretion, virus replication, receptor expression, has been examined by using flow cytometry, ELISA, Western-blot, confocal, and TCID50. Results: First, we found that porcine alveolar macrophages produced a great amount of soluble TNFα upon PRRSV infection, and this soluble TNFα in turn has great anti-PRRSV effect. By using inhibitor and genetic modification methods, we addressed that the production of porcine TNFα was mediated by ADAM17. Next, we found that inhibition of ADAM17 activity facilitated PRRSV infection in different target cells. Furthermore, we revealed that virus infection-activated ADAM17 can cleave PRRSV receptor CD163, which thus hinders virus entry. Lastly, we discovered that PRRSV treatment also can stimulate porcine neutrophils to produce soluble form of CD16(s CD16) in vivo and in vitro, which can serve as a biomarker for PRRSV infection. We then proved that the production of s CD16 is also an ADAM17-mediated ectodomain shedding event. Since we have shown that CD16 is involved in antibody-dependent enhancement(ADE) of PRRSV, this result indicates that the downregulation of CD16 might restrict CD16-mediated ADE effect of PRRS. Conclusion: PRRSV infection can stimulate ADAM17, which subsequently plays an anti-virus role through cleaving its substrates. Our findings suggest that activation of ADAM17 may be useful in enhancing the porcine anti-PRRSV response.
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