CARD9-mediated ambient PM2.5-induced pulmonary injury is associated with Th17 cell
CARD9-mediated ambient PM2.5-induced pulmonary injury is associated with Th17 cell
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CARD9介导的环境PM2.5诱导的肺损伤与Th17细胞相关
DOI：
10.1016/j.toxlet.2017.03.015
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发表时间：
2017-05-05
影响因子：
3.5
通讯作者：
Zhao, Jinzhuo
中科院分区：
文献类型：
--
作者：
Jiang, Shuo;Bo, Liang;Zhao, Jinzhuo
Inflammation and oxidative stress are important risk factors in PM2.5-induced injury. The current study attempted to study the role of caspase recruitment domain (CARD) 9 in ambient PM2.5-induced pulmonary injury in mice. The CARD9(-/-) and C57BL/6 mice were exposed to 3.6, 7.8 and 15.6 mg/kg bw of PM2.5 or saline by intratracheal instillation. After the last PM2.5 exposure, the spleen, bronchoalveolar lavage fluid (BALF) and pulmonary tissue were collected and examined. The results showed that PM2.5 exposure induced inflammatory cell infiltration and alveolar septal thickening in the lung. Regulatory T (Treg) cells in spleen of CARD9(-/-) mice were significantly higher than that in the C57BL/6 mice, whereas the T helper cells 17 (Th17) were lower. The levels of interleukin (IL)-6 and IL-17A in BALF of the CARD9(-/-) mice were significantly lower than that in the C57BL/6 mice. The mRNA expression of IL-17A, IL-6 and ROR gamma t in the lung of the CARD9(-/-) mice is significantly lower than that in the C57BL/ 6 mice, whereas the mRNA levels of Foxp3 in CARD9(-/-) mice were significantly higher than that in the C57BL/ 6 mice at the same dose of PM2.5. The protein expression of nuclear factor kB (NF-kappa B) is higher in the C57BL/ 6 mice than that in the CARD9(-/-) mice. This study indicates that ambient PM2.5-induced pulmonary injury is associated with the immune and inflammatory response. CARD9-mediated Th17/Treg differentiation probably played an important role in PM2.5-induced pulmonary damage. (C) 2017 Elsevier B.V. All rights reserved.
