CARD9-mediated ambient PM2.5-induced pulmonary injury is associated with Th17 cell

- Ambient PM2.5-induced pulmonary injury is associated with the immune and inflammatory response.
- PM2.5 induced the imbalance of Th17 and Treg.
- CARD9-mediated Th17/Treg differentiation played an important role in PM2.5-induced pulmonary damage.

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 RORγt 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 κB (NF-κB) 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.

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