国际呼吸杂志
國際呼吸雜誌
국제호흡잡지
INTERNATIONAL JOURNAL OF RESPIRATION
2011年
3期
177-181
,共5页
杜毅鹏%王伟%杨薇%贺蓓
杜毅鵬%王偉%楊薇%賀蓓
두의붕%왕위%양미%하배
气道炎症%慢性阻塞性肺疾病%炎症因子
氣道炎癥%慢性阻塞性肺疾病%炎癥因子
기도염증%만성조새성폐질병%염증인자
Airway inflammation%Chronic obstructive pulmonary disease%Inflammatory cytokines
目的 已有研究证实白介素32(IL-32)在慢性阻塞性肺疾病(COPD)患者肺组织中表达增高且与气流受限程度相关,提示IL-32可能与COPD的异常炎症反应和疾病进展有关.本研究拟观察沙美特罗氟替卡松对稳定期COPD患者IL-32表达的影响,探讨IL-32在COPD发病中的作用.方法 所有受试者共分为4组:稳定期COPD患者32例,健康吸烟者18人,健康非吸烟者18人.其中稳定期COPD患者随机分为2组,分别为接受沙美特罗/氟替卡松治疗(50μg/500μg,2次/d)及沙丁胺醇/异丙托溴铵(21μg/120μg,4次/d)治疗随访3个月,随访前后收集临床资料、肺功能、诱导痰、血浆,采用酶联免疫吸附试验方法检测诱导痰上清及血浆中IL-32及肿瘤坏死因子α(TNF-α)的浓度.结果 治疗前各组受试者间诱导痰及血浆中IL-32浓度及浓度的差异均无统计学意义.COPD组患者的诱导痰IL-32浓度与痰巨噬细胞及中性粒细胞计数、第1秒用力呼气容积(FEV1)占预计值百分比及圣乔治呼吸评分(SGRQ)均无相关性.COPD组血浆TNF-α浓度显著高于对照组且与血浆IL-32浓度呈正相关(r=0.65,P <0.001).治疗3个月后随访结果显示:两组患者治疗前后诱导痰及血浆IL-32浓度、诱导痰细胞总数、中性粒细胞计数、巨噬细胞计数及肺功能FEV1的差异均无统计学意义.沙美特罗/氟替卡松组治疗后SGRQ较治疗前显著下降,其差异有统计学意义(P<0.001),而沙丁胺醇/异丙托溴铵组治疗前后SGRQ无显著差异.结论 IL-32与COPD患者诱导痰炎症细胞增多无明显相关性,但可能参与了COPD全身炎症反应.沙美特罗/氟替卡松可改善COPD患者的临床症状并提高生活质量,但其对IL-32的表达无显著影响.
目的 已有研究證實白介素32(IL-32)在慢性阻塞性肺疾病(COPD)患者肺組織中錶達增高且與氣流受限程度相關,提示IL-32可能與COPD的異常炎癥反應和疾病進展有關.本研究擬觀察沙美特囉氟替卡鬆對穩定期COPD患者IL-32錶達的影響,探討IL-32在COPD髮病中的作用.方法 所有受試者共分為4組:穩定期COPD患者32例,健康吸煙者18人,健康非吸煙者18人.其中穩定期COPD患者隨機分為2組,分彆為接受沙美特囉/氟替卡鬆治療(50μg/500μg,2次/d)及沙丁胺醇/異丙託溴銨(21μg/120μg,4次/d)治療隨訪3箇月,隨訪前後收集臨床資料、肺功能、誘導痰、血漿,採用酶聯免疫吸附試驗方法檢測誘導痰上清及血漿中IL-32及腫瘤壞死因子α(TNF-α)的濃度.結果 治療前各組受試者間誘導痰及血漿中IL-32濃度及濃度的差異均無統計學意義.COPD組患者的誘導痰IL-32濃度與痰巨噬細胞及中性粒細胞計數、第1秒用力呼氣容積(FEV1)佔預計值百分比及聖喬治呼吸評分(SGRQ)均無相關性.COPD組血漿TNF-α濃度顯著高于對照組且與血漿IL-32濃度呈正相關(r=0.65,P <0.001).治療3箇月後隨訪結果顯示:兩組患者治療前後誘導痰及血漿IL-32濃度、誘導痰細胞總數、中性粒細胞計數、巨噬細胞計數及肺功能FEV1的差異均無統計學意義.沙美特囉/氟替卡鬆組治療後SGRQ較治療前顯著下降,其差異有統計學意義(P<0.001),而沙丁胺醇/異丙託溴銨組治療前後SGRQ無顯著差異.結論 IL-32與COPD患者誘導痰炎癥細胞增多無明顯相關性,但可能參與瞭COPD全身炎癥反應.沙美特囉/氟替卡鬆可改善COPD患者的臨床癥狀併提高生活質量,但其對IL-32的錶達無顯著影響.
목적 이유연구증실백개소32(IL-32)재만성조새성폐질병(COPD)환자폐조직중표체증고차여기류수한정도상관,제시IL-32가능여COPD적이상염증반응화질병진전유관.본연구의관찰사미특라불체잡송대은정기COPD환자IL-32표체적영향,탐토IL-32재COPD발병중적작용.방법 소유수시자공분위4조:은정기COPD환자32례,건강흡연자18인,건강비흡연자18인.기중은정기COPD환자수궤분위2조,분별위접수사미특라/불체잡송치료(50μg/500μg,2차/d)급사정알순/이병탁추안(21μg/120μg,4차/d)치료수방3개월,수방전후수집림상자료、폐공능、유도담、혈장,채용매련면역흡부시험방법검측유도담상청급혈장중IL-32급종류배사인자α(TNF-α)적농도.결과 치료전각조수시자간유도담급혈장중IL-32농도급농도적차이균무통계학의의.COPD조환자적유도담IL-32농도여담거서세포급중성립세포계수、제1초용력호기용적(FEV1)점예계치백분비급골교치호흡평분(SGRQ)균무상관성.COPD조혈장TNF-α농도현저고우대조조차여혈장IL-32농도정정상관(r=0.65,P <0.001).치료3개월후수방결과현시:량조환자치료전후유도담급혈장IL-32농도、유도담세포총수、중성립세포계수、거서세포계수급폐공능FEV1적차이균무통계학의의.사미특라/불체잡송조치료후SGRQ교치료전현저하강,기차이유통계학의의(P<0.001),이사정알순/이병탁추안조치료전후SGRQ무현저차이.결론 IL-32여COPD환자유도담염증세포증다무명현상관성,단가능삼여료COPD전신염증반응.사미특라/불체잡송가개선COPD환자적림상증상병제고생활질량,단기대IL-32적표체무현저영향.
Objective The interleukin-32(IL-32), a newly discovered cytokine, was reported to have increased expressions in the lung tissue of patients with chronic obstructive pulmonary disease (COPD) and correlated with the degree of airflow obstructions. This study was to undertake a randomized controlled trail to evaluate combined salmeterol/fluticasone on IL-32 and inflammatory cells in induced sputum and plasma of COPD patients and discuss whether IL-32 is related to the inflammatory disorder of COPD patients. Methods Using enzyme-linked immunosorbent assay, the expression of IL-32 in induced sputum and plasma was respectively examined to the following groups: 32 patients with stable COPD, 18 asymptomatic smokers, and 18 nonsmokers. COPD patients were treated in an open-labeled, randomized,parallel group and controlled trial with either a combination of 50 μg salmeterol and 500 μg fluticasone twice daily (SF, n = 18) or 21 μg salbutamol and 120 μg ipratropine quartic daily (IS, n = 18) for 3 months. At the start and end of treatment induced sputum was performed and the level of IL-32 was measured. Results IL-32 level in sputum and plasma of the four groups did not show significant differences. IL-32 level in sputum had no correlation to macrophage and neutrophil count in sputum,FEV1% predicted and SGRQ. IL-32 level in plasma of COPD patients had positive correlation to TNF-α level in plasma ( r=0. 65, P<0. 001). In addition, SGRQ was significantly reduced by SF ( P<0. 001)which was not seen with IS. SF did not significantly change IL-32 level in sputum and plasma,macrophage and neutrophil count in sputum and FEV1 % predicted compared with IS. Conclusions The results of this study suggested that although IL-32 was not related to the increase of inflammatory cells in induced sputum of COPD patients, it might be implicated in the systematic inflammatory disorder of COPD patients. SF improved the health status but did not significantly change IL-32 level and inflammatory cells in induced sputum of COPD patients.