Analysis of IL-6 mRNA expression in BALF cells from IPF patients

肺纤维化的发病机制可能与免疫效应细胞分泌炎性细胞因子有关。在这项研究中，从特发性间质性肺炎（IIP） （n=9）、石棉肺（n=4）、矽肺（n=8）、肺癌（n= 6）和健康志愿者（n=12）的支气管肺泡灌洗液（BALF）细胞中提取rna，并通过逆转录聚合酶链反应（RT-PCR）扩增来评估细胞因子的mrna。定量结果以细胞因子和β -肌动蛋白PCR产物的数量之比表示，作为内控。IIP、石棉肺、矽肺患者的tgf - β mRNA表达水平明显高于肺癌患者和健康志愿者。在这三种疾病的患者中，BALF细胞中il -1 β和TNFalpha mRNA的表达以及BALF中il -1 β蛋白滴度均受到抑制。肺纤维化患者与健康志愿者IL-8、IL-6 mRNA的表达差异无统计学意义。与健康志愿者相比，肺纤维化患者BALF中前列腺素E2 （PGE2）浓度较高。il -1 β和TNFalpha生成的减少可能部分是由于患者BALF中PGE2的高水平。这些结果表明，il -1 β、TNFalpha和tgf - β的调节机制可能在IIP、石棉沉滞和矽肺患者中是共同的，这些细胞因子可能显著促进肺泡损伤和随后的纤维化。为了研究细胞因子和生长因子在体内的生物学作用，我们计划利用hvj脂质体将tgf - β基因导入大鼠肺。

The pathogenesis of fibrosing lung disease likely involves inflammatory cytokines secreted from immune effector cells. In this study RNAs were extracted from bronchoalveolar lavage fluid (BALF) cells obtained from patients with idiopathic interstitial pneumonia (IIP) (n=9), asbestosis (n=4), silicosis (n=8), lung cancer( n=6) and healthy volunteers(n=12), and mRNAs for cytokines were assessed by amplofication with reverse transcription-polymerase chain reaction(RT-PCR). The quantitative results were expressed as ratios of the amount of PCR products of cytokines and beta-actin as an internal control. The expression of TGF-beta mRNA was elevated jin the patients with IIP, asbestosis and silicosis as compared with controls of the lung cancer patients and the healthy volunteers. The expressions of IL-1beta and TNFalpha mRNA in BALF cells and IL-1beta protein titer in BALF were both suppressed in the patients with these three diseases. No significant differences were observed in the expression of IL-8 or IL-6 mRNA between the patients with lung fibrosis and the healthy volunteers. Prostaglandin E2 (PGE2) concentration in BALF from patients with lung fibrosis was higher as compared to healthy volunteers. The decreases in IL-1beta and TNFalpha production may be, in part, due to high level of PGE2 in BALF from patients. These results suggest that regulatory mechanism (s) of IL-1beta, TNFalpha and TGF-beta may be common to patients with IIP, asbestosis and silicosis, and these cytokines may significantly contribute to the alveolar damage and subseqent fibrosis. To characterriza the biololgical roles of cytokines and growth-factors in vivo, we are planning to introduce TGFbeta gene into rat lung by using HVJ-liposome.