IL-17 Inversely Correlated with IL-10 via the STAT3 Gene in Pneumocystis-Infected Mice
IL-17 Inversely Correlated with IL-10 via the STAT3 Gene in Pneumocystis-Infected Mice
复制标题
在肺孢子虫感染的小鼠中，IL-17 通过 STAT3 基因与 IL-10 呈负相关
DOI：
10.1155/2019/6750861
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发表时间：
2019-09-10
影响因子：
4.6
通讯作者：
Tong, Zhao-Hui
中科院分区：
文献类型：
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作者：
Rong, Heng-Mo;Qian, Xiao-Jun;Tong, Zhao-Hui
背景肺孢子虫肺炎（PCP）仍然是免疫抑制个体中常见的机会性感染。目前的研究表明，多种免疫细胞和细胞因子参与了宿主对肺孢子虫（PC）的防御。然而，IL-17和IL-10在PCP发展中的作用尚未阐明。方法采用ELISA法检测PCP小鼠血清中IL-10和IL-17水平。通过流式细胞术检测IL-17-/- PCP小鼠肺中B10细胞、IL-10+巨噬细胞和IL-10+ T细胞以及IL-10-/- PCP小鼠中Th 17细胞和IL-17+γδT细胞的百分比。此外，还进行了抗体中和检查，以阐明PCP模型中IL-17和IL-10的关系。结果肺孢子虫感染小鼠血清中IL-17和IL-10水平明显升高。此外，IL-17或IL-10缺乏可导致肺孢子虫清除延迟和更严重的肺损伤。我们的数据还表明，IL-17缺乏提高了PCP小鼠血清IL-10水平和肺中B10细胞、IL-10+巨噬细胞和IL-10+ T细胞的百分比。有趣的是，我们还注意到IL-10-/- PCP小鼠血清中IL-17水平和肺中Th 17细胞和IL-17+γδT细胞百分比的增加。利用抗体中和实验，我们发现STAT 3基因可能在PCP中IL-17和IL-10的相互作用中起关键作用。结论IL-17和IL-10在PCP的发生发展过程中起保护作用，二者的负相关作用可能通过STAT 3介导。
Background Pneumocystis pneumonia (PCP) remains a common opportunistic infection in immunosuppressed individuals. Current studies showed that multiple immune cells and cytokines took part in the host defense against Pneumocystis (PC). However, the roles of IL-17 and IL-10 in the development of PCP have not been elucidated. Methods IL-10 and IL-17 levels in serum from PCP mice were detected via ELISA. The percentages of B10 cells, IL-10+ macrophages, and IL-10+ T cells in the lung from IL-17–/– PCP mice and Th17 cells and IL-17+γδT cells in IL-10–/– PCP mice were examined via flow cytometry. Also, antibody neutralization examination was also performed to elucidate the relationship of IL-17 and IL-10 in the PCP model. Results We noted the increase of IL-17 and IL-10 levels in serum from mice infected with Pneumocystis. Furthermore, deficiency of IL-17 or IL-10 could lead to the delayed clearance of Pneumocystis and more severed lung damage. Our data also demonstrated that IL-17 deficiency enhanced the serum IL-10 level and the percentages of B10 cells, IL-10+ macrophages, and IL-10+ T cells in the lung from PCP mice. Interestingly, we also noted an increase of the IL-17 level in serum and Th17 cell and IL-17+γδT cell percentages in the lung from IL-10–/– PCP mice. Using antibody neutralization experiments, we found that the STAT3 gene might play a critical role in the interplay of IL-17 and IL-10 in PCP. Conclusion Taken together, our results demonstrated that IL-17 and IL-10 could play the protective roles in the progression of PCP and the inverse correlation of them might be mediated by STAT3.