Volume 19 Issue 4
Apr.  2021
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Article Navigation >  Chinese Journal of General Practice  > 2021  >  19(4): 542-546
ZHONG Yu, SU Guo-mei, XIONG Zhi-lin, HUANG Tong, LUO Chao-le, LAI Tian-wen. PM-induced IL-17A expression enhances airway inflammation in cigarette-exposed mice[J]. Chinese Journal of General Practice, 2021, 19(4): 542-546. doi: 10.16766/j.cnki.issn.1674-4152.001856
Citation: ZHONG Yu, SU Guo-mei, XIONG Zhi-lin, HUANG Tong, LUO Chao-le, LAI Tian-wen. PM-induced IL-17A expression enhances airway inflammation in cigarette-exposed mice[J]. Chinese Journal of General Practice, 2021, 19(4): 542-546. doi: 10.16766/j.cnki.issn.1674-4152.001856
shu

PM-induced IL-17A expression enhances airway inflammation in cigarette-exposed mice

doi: 10.16766/j.cnki.issn.1674-4152.001856

  • Department of Respiratory and Critical Care Medicine, the Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong 524001, China

Funds:

 2018A0303130269

 2020B1515020004

  • Received Date: 2020-09-05
    Available Online: 2022-02-16
    Abstract
  •   Objective  This study aimed to investigate the mechanisms of atmospheric fine particulate matter (PM), which enhanced the inflammatory response in cigarette-exposed mice.  Methods  Wild-type and IL-17A knockout (IL-17A-/-) mice were randomly divided into the control group, smoked group, PM group and smoked+PM group according to the random number table method (6-8 mice/group). Mice were exposed to smoke using cigarette smoke exposure device. PM was inhaled by airway instillation, and airway inflammation was observed. After continuous intervention for 3 months, mice were sacrificed to measure airway inflammation. HE was used to detect inflammatory infiltration in lung tissue, and ELISA and RT-PCR were used to detect inflammatory cytokines in lung tissue. Smooth muscle expression was detected by immunohistochemistry, and collagen deposition was observed by Masson staining. In addition, IL-17A-secreting lymphocytes were detected by cell flow cytometry. In in vitro experiments, different concentrations of cigarette smoke extract (CSE) and/or PM were used to stimulate human airway epithelial (HBE) cells, and IL-17A siRNA was used to knock down IL-17A gene in HBE cells. RT-PCR detects the expression of inflammatory factors.  Results  Compared with the control, smoked and PM groups, lung tissue inflammatory factors (CXCL1, TFG-β1, IL-6 and IL-17A), collagen deposition and smooth muscle expression were significantly increased in the smoked+PM group. By contrast, IL-17A-/- mice can alleviate the above-mentioned indicators. Flow cytometry found that PM promoted IL-17A expression by regulating CD4 cells and worsened the inflammatory response induced by smoking. In vitro, CSE or PM intervention in HBE cells can induce the secretion of IL-6 and IL-8, whereas CSE combined with PM can further increase the expression of IL-6 and IL-8. Knockout of IL-17A gene in HBE cells can alleviate the expression of IL-6 and IL-8.  Conclusion  PM can induce the expression of IL-17A and exacerbate the inflammation, collagen deposition and smooth muscle hyperplasia in the lung tissue of cigarette-exposed mice, suggesting that targeted therapy for the IL-17A signalling pathway may be effective in relieving acute exacerbation of COPD caused by PM.

     

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