Sagwal Swati, Prasad Rajendra, Kaur Jyotdeep, Singh Meenu
Department of Pediatrics, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.
Department of Biochemistry, Maharishi Markandeswar Institute of Medical Sciences and Research, Ambala, Haryana, India.
Mol Cell Biochem. 2021 Jul;476(7):2869-2876. doi: 10.1007/s11010-021-04051-2. Epub 2021 Mar 19.
This was an observational cross-sectional study which was done to assess the expression profile of STATs and SOCS genes in cystic fibrosis. The mRNA was isolated from peripheral blood mononuclear cells of CF patients in exacerbation, colonization and post exacerbation phases of the disease. The relative gene expression level for SOCS 1, -3, -5 and STAT 1, -3,-4,-6 genes was quantified by Real-time PCR. The levels of IL-6 were also measured in the serum by ELISA. The expression of the Th1 pathway associated genes (SOCS1, SOCS5, STAT4 and STAT1) was downregulated while the expression of Th2/Th17 pathway genes (SOCS3, STAT3, STAT6) was upregulated in both exacerbation and colonization phases as compared to healthy controls. The serum levels of IL-6 were also elevated in both the disease groups. After antibiotic treatment, the expression of SOCS5 and STAT4 was increased while the expression of rest of the genes showed downregulation which shows a shift in immune response from Th2/Th17 to Th1. Our results suggest that infection alters the cytokine signaling pathway through modulation of STATs and SOCS genes which is not able to regulate the overstimulation of cytokine signaling further leading to chronic inflammation in CF.
这是一项观察性横断面研究，旨在评估囊性纤维化中信号转导和转录激活因子（STATs）及细胞因子信号抑制因子（SOCS）基因的表达谱。从处于疾病加重期、定植期和加重期后阶段的囊性纤维化患者外周血单个核细胞中分离mRNA。通过实时聚合酶链反应（Real-time PCR）定量SOCS 1、-3、-5以及STAT 1、-3、-4、-6基因的相对基因表达水平。还通过酶联免疫吸附测定（ELISA）法检测血清中白细胞介素-6（IL-6）的水平。与健康对照相比，在加重期和定植期，Th1途径相关基因（SOCS1、SOCS5、STAT4和STAT1）的表达下调，而Th2/Th17途径基因（SOCS3、STAT3、STAT6）的表达上调。两个疾病组的血清IL-6水平也升高。抗生素治疗后，SOCS5和STAT4的表达增加，而其余基因的表达下调，这表明免疫反应从Th2/Th17向Th1转变。我们的结果表明，感染通过调节STATs和SOCS基因改变细胞因子信号通路，而这无法进一步调节细胞因子信号的过度刺激，从而导致囊性纤维化中的慢性炎症。
