CAJ | 학술논문

目的探讨不同炎症表型哮喘患者治疗后血浆及诱导痰中抗菌肽LL-37水平的变化及其意义.方法研究对象为2009年8月至2010年8月南方医科大学南方医院初诊的34例非急性发作期哮喘患者(哮喘组)和同期14名行健康体检者(对照组).所有研究对象均行外周血、诱导痰细胞分类,留取血浆、痰上清.根据诱导痰嗜酸粒细胞(EOS)计数将哮喘组分为EOS型(≥3％)及非EOS型(＜3％).哮喘组采用布地奈德/福莫特罗(160/4.5 μg,1吸,2次/d)治疗1个月后复查上述指标.应用酶联免疫吸附测定( ELISA)法检测哮喘组治疗前、后及对照组的血浆、痰上清液LL-37水平.结果治疗前哮喘组血浆、痰LL-37水平[数据以M(QR)表示,下同][5.0(9.2)、28.4( 109.8)μg/L]与对照组[2.4(11.4)、34.5(57.8)μg/L]差异无统计学意义(P=0.427、0.427),血浆LL-37水平与第1秒用力呼气容积(FEV1)、FEV1占预计值百分比(FEV1％预计值)、用力肺活量(FVC)呈负相关(r=-0.470、-0.421、-0.367,P=0.005、0.013、0.033).治疗后哮喘组血浆、痰LL-37水平[5.6(16.2)、65.6(184.0).μg/L]高于治疗前(P =0.005、0.015),其中EOS型患者显著增高[5.3(19.3)比6.7(8.9) μg/L,P=0.021；65.6(185.2)比35.3( 102.0) μg/L,P=0.014],而非EOS型患者无明显变化(P =0.139、0.386).治疗后哮喘组血浆LL-37水平与FEV1、FEV1％预计值、FVC无显著相关性(P=0.283、0.706、0.272).结论 LL-37可能参与了哮喘病情的加重,而EOS型哮喘治疗后LL-37的增加可能与治疗解除了EOS炎症对LL-37表达的抑制有关,其机制有待进一步研究.
목적 탐토불동염증표형효천환자치료후혈장급유도담중항균태LL-37수평적변화급기의의.방법 연구대상위2009년8월지2010년8월남방의과대학남방의원초진적34례비급성발작기효천환자(효천조)화동기14명행건강체검자(대조조).소유연구대상균행외주혈、유도담세포분류,류취혈장、담상청.근거유도담기산립세포(EOS)계수장효천조분위EOS형(≥3％)급비EOS형(＜3％).효천조채용포지내덕/복막특라(160/4.5 μg,1흡,2차/d)치료1개월후복사상술지표.응용매련면역흡부측정( ELISA)법검측효천조치료전、후급대조조적혈장、담상청액LL-37수평.결과 치료전효천조혈장、담LL-37수평[수거이M(QR)표시,하동][5.0(9.2)、28.4( 109.8)μg/L]여대조조[2.4(11.4)、34.5(57.8)μg/L]차이무통계학의의(P=0.427、0.427),혈장LL-37수평여제1초용력호기용적(FEV1)、FEV1점예계치백분비(FEV1％예계치)、용력폐활량(FVC)정부상관(r=-0.470、-0.421、-0.367,P=0.005、0.013、0.033).치료후효천조혈장、담LL-37수평[5.6(16.2)、65.6(184.0).μg/L]고우치료전(P =0.005、0.015),기중EOS형환자현저증고[5.3(19.3)비6.7(8.9) μg/L,P=0.021；65.6(185.2)비35.3( 102.0) μg/L,P=0.014],이비EOS형환자무명현변화(P =0.139、0.386).치료후효천조혈장LL-37수평여FEV1、FEV1％예계치、FVC무현저상관성(P=0.283、0.706、0.272).결론 LL-37가능삼여료효천병정적가중,이EOS형효천치료후LL-37적증가가능여치료해제료EOS염증대LL-37표체적억제유관,기궤제유대진일보연구.
Objective To explore the post-therapeutic change of cathelicidin LL-37 in asthmatics of different inflammatory phenotypes.Methods Thirty-four patients with initially diagnosed asthma (asthma group) and 14 normal subjects (control group) were recruited at Nanfang Hospital from August 2009 to August 2010 for this prospective study.Sputum and venous blood samples were collected and analyzed for cell differential.Eosinophilic asthma was defined as the count of sputum eosinophils ≥ 3％.The LL-37 concentrations in plasma and sputum supernatant were measured by enzyme-linked immunosorbent assay (ELJSA) kit.The subjects were treated with budesonide/formoterol (160/4.5 μg) one inhalation twice daily and re-examined after 1 month.Results Prior to treatment,there were no differences between the asthma and control groups in the levels of LL-37 in plasma and sputum supernatant (P =0.427,0.427 ).The plasma concentrations of LL-37 in asthma group were negatively correlated with baseline forced expiratory volume in one second ( FEV1,r =- 0.470,P =0.005 ),percent predicted of FEV1 ( FEV1 ％ pred,r=-0.421,P=0.013) and forced vital capacity (FVC,r=-0.367,P =0.033). After treatment,the plasma and sputum supernatant concentrations of LL-37 (M (QR)) in the asthma group (5.6(16.2),65.6 (184.0) μg/L) were significantly higher than those baseline concentrations (5.0(9.2),28.4(109.8) μg/L,P =0.005,0.015).In the eosinophilic asthma subgroup,the plasma and sputum supernatant concentrations of LL-37 ( M ( QR ) ) after treatment ( 5.3 ( 19.3 ),65.6 (185.2) μg/L) were significantly higher than those baseline concentrations ( 6.7 ( 8.9 ),35.3 ( 102.0 ) μg/L,P =0.021,0.014 ). And in the non-eosinophilic asthma subgroup,the changes of plasma and sputum supernatant concentrations of LL-37 showed no significant differences (P =0.139,0.386).In the asthma group,the correlations between plasma concentrations of LL-37 and FEV1,FEV1 ％ pred,FVC were not statistically significant ( P =0.283,0.706,0.272 ) after treatment. Conclusions LL-37 may participate in the aggravation of asthma. The elevated concentrations of LL-37 in eosinophilic asthma is probably due to the resolved suppression of LL-37 expression by eosinophilic inflammation. But its mechanism needs further researches.