血清颗粒蛋白前体在慢性阻塞性肺疾病的表达及病情评估的临床价值

被引:11
作者
王娜
朱述阳
机构
[1] 徐州医科大学附属医院呼吸科
关键词
颗粒蛋白前体; 慢性阻塞性肺疾病; 炎性机制;
D O I
暂无
中图分类号
R563.9 [其他];
学科分类号
100201 [内科学];
摘要
目的探讨血清颗粒蛋白前体(PGRN)在慢性阻塞性肺疾病(COPD)的表达及病情评估的临床价值。方法选取COPD组患者86例,其中COPD急性加重期(AECOPD)51例、COPD稳定期患者(SCOPD)35例,同期健康对照组30例,入组后24 h内血清采用酶联免疫吸附法测定血清PGRN浓度,收集COPD患者临床资料并分析其与血清PGRN浓度的相关性。结果 COPD组血清PGRN浓度较健康对照组显著降低,3组间差异有统计学意义(F=149.419,P<0.05)。且AECOPD组血清PGRN浓度较SCOPD组显著升高。在AECOPD组中,呼吸衰竭者血清PGRN浓度较无呼吸衰竭者显著增高(t=-2.63,P=0.012)。血清PGRN浓度与白细胞计数、中性粒细胞计数、CAT评分、急性期C-反应蛋白呈显著正相关;与用力肺活量、第1秒用力呼气容积、第1秒用力呼气容积占预计值百分比、急性期嗜酸粒细胞计数呈显著负相关。结论 PGRN在COPD急性加重期起抗炎作用,与COPD病情评估多个指标存在相关性,可作为COPD病情严重程度的预测指标。
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共 10 条
[1]
Progranulin: A key player in autoimmune diseases.[J].Jinlong Jian;Guangfei Li;Aubryanna Hettinghouse;Chuanju Liu.Cytokine.2018,
[2]
Impact and associations of eosinophilic inflammation in COPD: analysis of the AERIS cohort [J].
Kim, Viktoriya L. ;
Coombs, Ngaire A. ;
Staples, Karl J. ;
Ostridge, Kristoffer K. ;
Williams, Nicholas P. ;
Wootton, Stephen A. ;
Devaster, Jeanne-Marie ;
Aris, Emmanuel ;
Clarke, Stuart C. ;
Tuck, Andrew C. ;
Bourne, Simon C. ;
Wilkinson, Tom M. A. .
EUROPEAN RESPIRATORY JOURNAL, 2017, 50 (04)
[3]
Blood eosinophil count and exacerbation risk in patients with COPD [J].
Kerkhof, Marjan ;
Sonnappa, Samatha ;
Postma, Dirkje S. ;
Brusselle, Guy ;
Agusti, Alvar ;
Anzueto, Antonio ;
Jones, Rupert ;
Papi, Alberto ;
Pavord, Ian ;
Pizzichini, Emilio ;
Popov, Todor ;
Roche, Nicolas ;
Ryan, Dermot ;
Thomas, Mike ;
Vogelmeier, Claus ;
Chisholm, Alison ;
Freeman, Daryl ;
Bafadhel, Mona ;
Hillyer, Elizabeth V. ;
Price, David B. .
EUROPEAN RESPIRATORY JOURNAL, 2017, 50 (01)
[4]
Cardiac Surgery Anesthesia And Systemic Inflammatory Response..[J].Sheikhi Mohammad Ali;Ebadi Ahmad;Shahriary Alireza;Davoodzadeh Hannaneh;Rahmani Hossein.International journal of bioassays.2015, 2
[5]
Prevention of LPS-Induced Acute Lung Injury in Mice by Progranulin.[J].Zhongliang Guo;Qinchuan Li;Yang Han;Yongjie Liang;Zengguang Xu;Tao Ren;Eeva Moilanen.Mediators of Inflammation.2012,
[6]
Granulin Is a Soluble Cofactor for Toll-like Receptor 9 Signaling [J].
Park, Boyoun ;
Buti, Ludovico ;
Lee, Sungwook ;
Matsuwaki, Takashi ;
Spooner, Eric ;
Brinkmann, Melanie M. ;
Nishihara, Masugi ;
Ploegh, Hidde L. .
IMMUNITY, 2011, 34 (04) :505-513
[7]
Proteinase 3 and neutrophil elastase enhance inflammation in mice by inactivating antiinflammatory progranulin [J].
Kessenbrock, Kai ;
Froehlich, Leopold ;
Sixt, Michael ;
Laemmermann, Tim ;
Pfister, Heiko ;
Bateman, Andrew ;
Belaaouaj, Azzaq ;
Ring, Johannes ;
Ollert, Markus ;
Faessler, Reinhard ;
Jenne, Dieter E. .
JOURNAL OF CLINICAL INVESTIGATION, 2008, 118 (07) :2438-2447
[8]
The neutrophil in chronic obstructive pulmonary disease [J].
Quint, Jennifer Kathleen ;
Wedzicha, Jadwiga Anna .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2007, 119 (05) :1065-1071
[9]
Conversion of Proepithelin to Epithelins.[J].Jing Zhu;Carl Nathan;Wenwen Jin;Davis Sim;Gillian S. Ashcroft;Sharon M. Wahl;Lynne Lacomis;Hediye Erdjument-Bromage;Paul Tempst;Clifford D. Wright;Aihao Ding.Cell.2002, 6
[10]
RNA expression patterns change dramatically in human neutrophils exposed to bacteria [J].
Subrahmanyam, YVBK ;
Yamaga, S ;
Prashar, Y ;
Lee, HH ;
Hoe, NP ;
Kluger, Y ;
Gerstein, M ;
Goguen, JD ;
Newburger, PE ;
Weissman, SM .
BLOOD, 2001, 97 (08) :2457-2468