Interleukin-10 Promotes Porcine Circovirus Type 2 Persistent Infection in Mice and Aggravates the Tissue Lesions by Suppression of T Cell Infiltration
Interleukin-10 Promotes Porcine Circovirus Type 2 Persistent Infection in Mice and Aggravates the Tissue Lesions by Suppression of T Cell Infiltration
复制标题
Interleukin-10促进小鼠猪圆环病毒2型持续感染并通过抑制T细胞浸润加重组织病变
DOI：
10.3389/fmicb.2019.02050
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发表时间：
2019-09-10
影响因子：
5.2
通讯作者：
Huang, Yong
中科院分区：
文献类型：
--
作者：
Du, Qian;Zhang, Huan;Huang, Yong
白细胞介素（IL）-10，作为一个关键的抗炎细胞因子，在猪圆环病毒2型（PCV 2）感染过程中增加，但IL-10在这个过程中的作用仍有待确定。在本研究中，使用IL-10缺陷小鼠模型，我们发现IL-10缺陷防止由PCV 2诱导的脾淋巴细胞（CD 45+细胞）减少，并通过诱导更多的T细胞趋化因子（CCL 3、CXCL 9和CXCL 10）来促进肺中的CD 4+和CD 8 + T细胞浸润。同时，PCV 2感染诱导IL-10缺陷小鼠中促炎细胞因子和PCV 2特异性抗体比野生型小鼠显著增加，导致IL-10缺陷小鼠肺中病毒载量较低，肺病变相对于野生型小鼠较轻。此外，肺CD 4+和CD 8 + T细胞的数量都与肺部病变以及PCV 2的病毒载量呈负相关。这些结果表明，PCV 2感染利用IL-10阻断T细胞向小鼠肺的转移，并且IL-10减弱促炎细胞因子和PCV 2特异性抗体的产生。T细胞浸润、促炎细胞因子和PCV 2特异性抗体的缺乏促进PCV 2复制，导致小鼠中更严重的肺部病变。
Interleukin (IL)-10, as a key anti-inflammatory cytokine, increases during porcine circovirus type 2 (PCV2) infection, but the role of IL-10 in the process remains to be defined. In the present study, using an IL-10 deficient mice model, we found that IL-10 deficiency prevented the reduction of splenic lymphocytes (CD45+ cells) induced by PCV2 and promoted CD4+ and CD8+ T cell infiltration in lungs through inducting more T cell chemokines (CCL3, CXCL9, and CXCL10). Simultaneously, PCV2 infection induced a significant increase of pro-inflammatory cytokines and PCV2-specific antibodies in IL-10 deficient mice than in wild-type mice, resulting in a lower viral load in lung and a milder lung lesion in IL-10 deficient mice relative to wild-type mice. Moreover, the amounts of pulmonary CD4+ and CD8+ T cells were all inversely correlated with the lung lesions, as well as the viral load of PCV2. These results demonstrate that PCV2 infection employs IL-10 to block the transfer of T cells to the lungs of mice, and IL-10 attenuates the production of pro-inflammatory cytokines and PCV2-specific antibodies. The lack of T cell infiltration, pro-inflammatory cytokines, and PCV2-specific antibodies promote PCV2 replication, leading to a more severe lung lesion in mice.