Human rhinovirus induced cytokine/chemokine responses in human airway epithelial and immune cells.
Human rhinovirus induced cytokine/chemokine responses in human airway epithelial and immune cells.
复制标题
DOI：
10.1371/journal.pone.0114322
复制
发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Anderson LJ
中科院分区：
文献类型：
--
作者：
Rajan D;McCracken CE;Kopleman HB;Kyu SY;Lee FE;Lu X;Anderson LJ
人鼻病毒（HRV）感染通常与急性上呼吸道和下呼吸道疾病以及哮喘恶化相关。HRV在这些疾病中发挥的作用表明，了解导致发病机制的宿主特异性或病毒特异性因素非常重要。由于A种HRV通常与比B种HRV更严重的HRV疾病相关，因此它们诱导的免疫应答的差异应告知疾病发病机制。为了鉴定诱导应答的种属差异，我们通过将人PBMC暴露于HRV感染的Calu-3细胞来评价3种A病毒（HRV 25、31和36）和3种B病毒（HRV 4、35和48）。为了评估先前HRV感染诱导的记忆对研究反应的潜在影响，我们测试了应该是HRV初治的脐带血单核细胞。对于IP-10和IL-15的一个或多个HRV，存在HRV相关增加（与模拟感染细胞相比显著增加），其不受添加PBMC的影响，对于MIP-1α、MIP-1β、IFN-α和HGF仅添加PBMC，以及对于ENA-78仅不添加PBMC。与A HRV相比，所有三种物种B HRV均诱导较高水平的MIP-1α和MIP-1β与PBMC以及ENA-78与PBMC。相反，添加CBMCs的效果较小，并且不诱导MIP-1α、MIP-1β或IFN-α，也不阻断ENA-78的产生。然而，添加CBMCs确实增加了HRV 35和HRV 36感染的IP-10水平。对于某些反应，存在对PBMC的影响而对CBMC无影响，表明两种类型细胞之间存在差异，可能是因为PBMC而非CBMC中存在HRV记忆反应，或者未成熟CBMC相对于PBMC的反应能力有限。因此，我们的研究结果表明，不同的HRV毒株可以诱导不同的细胞因子和趋化因子的模式;这些差异中的一些可能是由于过去的HRV感染引起的记忆反应的差异，以及其他与病毒因素相关的差异，可以告知疾病的发病机制。
Infections with human rhinovirus (HRV) are commonly associated with acute upper and lower respiratory tract disease and asthma exacerbations. The role that HRVs play in these diseases suggests it is important to understand host-specific or virus-specific factors that contribute to pathogenesis. Since species A HRVs are often associated with more serious HRV disease than species B HRVs, differences in immune responses they induce should inform disease pathogenesis. To identify species differences in induced responses, we evaluated 3 species A viruses, HRV 25, 31 and 36 and 3 species B viruses, HRV 4, 35 and 48 by exposing human PBMCs to HRV infected Calu-3 cells. To evaluate the potential effect of memory induced by previous HRV infection on study responses, we tested cord blood mononuclear cells that should be HRV naïve. There were HRV-associated increases (significant increase compared to mock-infected cells) for one or more HRVs for IP-10 and IL-15 that was unaffected by addition of PBMCs, for MIP-1α, MIP-1β, IFN-α, and HGF only with addition of PBMCs, and for ENA-78 only without addition of PBMCs. All three species B HRVs induced higher levels, compared to A HRVs, of MIP-1α and MIP-1β with PBMCs and ENA-78 without PBMCs. In contrast, addition of CBMCs had less effect and did not induce MIP-1α, MIP-1β, or IFN-α nor block ENA-78 production. Addition of CBMCs did, however, increase IP-10 levels for HRV 35 and HRV 36 infection. The presence of an effect with PBMCs and no effect with CBMCs for some responses suggest differences between the two types of cells possibly because of the presence of HRV memory responses in PBMCs and not CBMCs or limited response capacity for the immature CBMCs relative to PBMCs. Thus, our results indicate that different HRV strains can induce different patterns of cytokines and chemokines; some of these differences may be due to differences in memory responses induced by past HRV infections, and other differences related to virus factors that can inform disease pathogenesis.
登录
查看更多内容
影响因子：
4.6
作者：
Lenarczyk, A;Helsloot, J;Kirkham, B
通讯作者：
Kirkham, B
影响因子：
8
作者：
通讯作者：
--
DOI：
10.1016/j.jaci.2008.10.007
发表时间：
2009-01
期刊：
The Journal of allergy and clinical immunology
影响因子：
--
作者：
Miller EK;Edwards KM;Weinberg GA;Iwane MK;Griffin MR;Hall CB;Zhu Y;Szilagyi PG;Morin LL;Heil LH;Lu X;Williams JV;New Vaccine Surveillance Network
通讯作者：
New Vaccine Surveillance Network
影响因子：
3.6
作者：
Garcia, Carla;Soriano-Fallas, Alejandra;Mejias, Asuncion
通讯作者：
Mejias, Asuncion
影响因子：
3.6
作者：
Louie, Janice K.;Roy-Burman, Arup;Schnurr, David P.
通讯作者：
Schnurr, David P.