Abstract：Objective: To investigate the changes of plasma interleukin-17 and C-reactive protein(CRP) with acute exacerbation and remission of chronic obstructive pulmonary disease (COPD), and analyze its clinical significance. Methods: Thirty-five patients with acute exacerbation of COPD(COPD group) and 23 healthy subjects (control group) were enrolled in the study. The plasma CRP and IL-17 levels in two groups were measured and analysed. Results: The levels of plasma CRP and IL-17 from patients with acute exacerbation and remission of COPD were higher than that in healthy control group(both P<0.01). Analysis results indicated that plasma IL-17 was positively correlated with CRP in patients with acute exacerbation of COPD before treatment(r=0.402,P=0.001). Conclusion: IL-17 and CRP both involved in the acute inflammation of COPD, and combination of them had certain clinical significance in determining the acute exacerbation of COPD.
收稿日期: 2013-05-03
通讯作者:
柏宏坚，副教授，硕士生导师，主任医师，Email：thc822@163.com
作者简介: 唐海成（1979—），男，江苏盐城人，硕士，主治医师,主要从事呼吸系统疾病研究；
引用本文:
唐海成, 柏宏坚, 姜永前, 张群. 慢性阻塞性肺疾病患者血浆白介素-17、C反应蛋白的表达及相关性研究[J]. 江苏大学学报:医学版, 2013, 23(4): 325-327.
TANG Hai-cheng, BAI Hong-jian, JIANG Yong-qian, ZHANG Qun. Expression and correlation of plasma interleukin-17 and C-reactive protein in patients with chronic obstructive pulmonary disease. Journal of Jiangsu University(Medicine Edition), 2013, 23(4): 325-327.
[1]Zhong N, Wang C, Yao W, et al. Prevalence of chronic obstructive pulmonary disease in China: a large, population-based survey［J］. Am J Respir Crit Care Med, 2007, 176(8):753-760.[2]Sethi S, Wrona C, Eschberger K, et al. Inflammatory profile of new bacterial strain exacerbations of chronic obstructive pulmonary disease［J］. Am J Respir Crit Care Med, 2008, 177(5):491-497.[3]中华医学会呼吸病学分会慢性阻塞性肺疾病学组.慢性阻塞性肺疾病诊治指南(2007年修订版)［J］. 中华结核和呼吸杂志, 2007, 30(1):8-17.[4]Anthonisen NR, Manfreda J, Warren CP, et al. Antibiotic therapy in exacerbations of chronic obstructive pulmonary disease［J］. Ann Intern Med, 1987,106(2):196-204.[5]Sethi S, Murphy TF. Infection in the pathogenesis and course of chronic obstructive pulmonary disease［J］. N Engl J Med, 2008, 359(22):2355-2365.[6]Wrodycki W. Usefulness of plasma proealeitonin(PCT) estimation to diagnose patients in departments of infectious diseases［J］. Przegl Epidemiol, 2003, 57(1):211-219.[7]Wilkinson TM, Hurst JR, Perera WR, et al. Effect of interactions between lower airway bacterial and rhinoviral infection in exacerbations of COPD［J］. Chest， 2006,129(2):317-324.[8]Assicot M, Gendrel D, Carsin H, et al. High serum procalcitonin concentrations in patients with sepsis and infection［J］. Lancet, 1993, 341(8844):515-518.[9]Miyamoto M, Prause O, Sjstrand M, et al. Endogenous IL-17 as a mediator of neutrophil recruitment caused by endotoxin exposure in mouse airways ［J］. J Immunol, 2003, 170 (9):4665-4672.[10]Kofoed K, Andersen O, Kronborg G, et al. Use of plasma c-reactive protein, procalcitonin, neutrophils, macrophage migration inhibitory factor, soluble urokinasetype plasminogen activator receptor, and soluble triggering receptor expressed on myeloin cells-1 in combination to diagnose infections: a prospective study［J］. Crit Care Med， 2007,11(2):R38.
2013, Vol. 23 
