亚地诺病毒通过触发巨细胞两极分化和通过NF-κB激活激发IL-6的产生诱导儿科肺炎
Xiaoping Yuan1, Haoying Huang2, Huifeng Fan3
1Department of Respiratory Medicine, School of Pharmaceutical Sciences, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangdong Provincial Research Center for Child Health, Guangzhou 510623, China; Guangzhou Women and Children's Medical Center, Guangdong Provincial Research Center for Child Health, State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou 510623, China.
儿童感染人类腺病毒 (HAdV) 驱动M1巨细胞两极分化,通过NF-κB信号增加IL-6的产生. 这种机制有助于HAdV肺炎中严重的肺损伤.
科学领域:
- 免疫学 免疫学 免疫学
- 病毒学 病毒学
- 儿科呼吸道疾病 儿科呼吸道疾病
背景情况:
- 肺巨细胞是抗病毒防御和肺病原发生的关键.
- 在腺病毒引起的肺损伤中,巨细胞两极分化的作用尚未完全理解.
研究的目的:
- 调查HAdV肺炎儿童巨细胞两极分化的作用.
- 为了阐明HAdV诱导的肺损伤的分子机制.
主要方法:
- 支气管支气管洗液 (BALF) 细胞的大量RNA测序.
- 对巨细胞群体的流细胞计分析.
- 人类巨细胞系的体外感染.
主要成果:
- 腺病毒感染可以提高与巨细胞两极分化相关的基因的调节.
- 严重的HAdV肺炎病例中,M1巨细胞的比例更高.
- 在体外,HAdV通过NF-κB激活直接诱导M1极化和IL-6的产生.
结论:
- HAdV感染促进了M1巨细胞的两极分化和IL-6的释放.
- NF-κB信号传递是HAdV驱动的炎症和肺损伤中的关键途径.
- 了解这种机制可以了解严重的HAdV感染病原体.
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