CCL3 and Viral Chemokine-Binding Protein gG Modulate Pulmonary Inflammation and Virus Replication during Equine Herpesvirus 1 Infection
CCL3 and Viral Chemokine-Binding Protein gG Modulate Pulmonary Inflammation and Virus Replication during Equine Herpesvirus 1 Infection
复制标题
CCL3 和病毒趋化因子结合蛋白 gG 调节马疱疹病毒 1 感染期间的肺部炎症和病毒复制
DOI：
10.1128/jvi.02137-07
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发表时间：
2007
影响因子：
5.4
通讯作者：
N. Osterrieder
中科院分区：
文献类型：
--
作者：
G. R. Van de Walle;K. Sakamoto;N. Osterrieder
摘要CCL 3是一种促炎趋化因子，介导肺部疾病中发生的许多细胞变化。在这里，CCL 3 −/−小鼠被用来研究这种趋化因子在呼吸道疱疹病毒感染过程中的作用。与野生型小鼠相比，感染α疱疹病毒马疱疹病毒1型（EHV-1）的CCL 3 −/−小鼠体重减轻，但肺部病毒载量较高。感染CCL 3 −/−小鼠的肺部遭受了较轻的间质性肺炎，感染后从肺气道中回收的免疫细胞较少。我们还可以证明疱疹病毒编码的趋化因子结合糖蛋白G（gG）能够抑制CCL 3的趋化功能。然而，这种CCL 3介导的趋化性在gG特异性抗体存在下恢复，这对gG缺失突变体作为标记疫苗的广告用途提出了质疑。总之，我们得出结论，CCL 3是控制疱疹病毒在靶器官肺中复制的主要参与者，并且通过引起强烈的炎症反应来实现。CCL 3的免疫调节活性通过病毒gG的表达来平衡，其趋化因子结合活性在继发性感染中通过产生抗gG抗体来减轻。
ABSTRACT CCL3 is a proinflammatory chemokine that mediates many of the cellular changes occurring in pulmonary disease. Here, CCL3−/− mice were used to investigate the role of this chemokine during respiratory herpesvirus infection. Compared to wild-type mice, CCL3−/− mice infected with the alphaherpesvirus equine herpesvirus 1 (EHV-1) displayed reduced body weight loss but had higher pulmonary viral loads. Lungs from infected CCL3−/− mice suffered a milder interstitial pneumonia, and fewer immune cells were recovered from the pulmonary airways after infection. We could also demonstrate that herpesvirus-encoded chemokine-binding glycoprotein G (gG) was capable of inhibiting the chemotactic functions of CCL3. This CCL3-mediated chemotaxis, however, was restored in the presence of gG-specific antibodies, which puts into question the advertised use of gG deletion mutants as marker vaccines. In summary, we concluded that CCL3 is a major player in controlling herpesvirus replication in the target organ, the lung, and does so by evoking a strong inflammatory response. The immunomodulatory activity of CCL3 is balanced by the expression of viral gG, whose chemokine-binding activity is mitigated in secondary infections by the production of anti-gG antibodies.
巨噬细胞炎症蛋白 1 α 介导小鼠内毒素血症的肺白细胞募集、肺毛细血管渗漏和早期死亡率。
DOI：
--
发表时间：
1995
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Standiford,TJ;Kunkel,SL;Lukacs,NW;Greenberger,MJ;Danforth,JM;Kunkel,RG;Strieter,RM
通讯作者：
Strieter,RM
间质性肺疾病中巨噬细胞炎症蛋白 1 α 的表达。
DOI：
--
发表时间：
1993
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Standiford,TJ;Rolfe,MW;Kunkel,SL;Lynch3rd,JP;Burdick,MD;Gilbert,AR;Orringer,MB;Whyte,RI;Strieter,RM
通讯作者：
Strieter,RM
影响因子：
56.9
作者：
COOK, DN;BECK, MA;SMITHIES, O
通讯作者：
SMITHIES, O