临床儿科杂志
臨床兒科雜誌
림상인과잡지
2014年
3期
261-264
,共4页
哮喘%嗜酸性粒细胞%干细胞因子%卡介苗
哮喘%嗜痠性粒細胞%榦細胞因子%卡介苗
효천%기산성립세포%간세포인자%잡개묘
asthma%eosinophils%stem cell factor%Bacillus Calmette-Guerin
目的：研究卡介苗（BCG）对哮喘小鼠干细胞因子（SCF）表达的影响。方法昆明小鼠随机分为哮喘组、BCG组和对照组，每组10只，以卵清蛋白（OVA）致敏激发建立哮喘模型。末次激发24 h后取肺组织及支气管肺泡灌洗液（BALF），计数嗜酸性粒细胞（EOS）；酶联免疫吸附法检测BALF中SCF水平；免疫组织化学图像分析技术测定肺组织中SCF蛋白表达。结果哮喘组、BCG组和对照组肺组织的EOS计数分别为（10.67±1.94）个/HP（、6.40±1.55）个/HP和（0.37±0.33）个/HP，BALF中EOS计数分别为（7.58±1.30）×107/L、（3.78±1.15）×107/L和0，三组间差异有统计学意义（P均<0.01）。哮喘组、BCG组和对照组的肺组织SCF蛋白免疫组化指数分别为（24787.97±7214.12）（、20509.50±4775.27）和（12261.66±3277.65），BALF中SCF水平分别为（280.25±14.20）pg/ml、（266.77±31.15）pg/ml和（223.59±15.61）pg/ml，其中哮喘组和BCG组均高于对照组，差异有统计学意义（P均<0.05），BCG组与哮喘组差异无统计学意义（P>0.05）。哮喘组肺部SCF表达与EOS计数呈正相关（P<0.05）。结论 BCG干预能显著减轻哮喘小鼠的气道炎症，但不能抑制SCF的表达。
目的：研究卡介苗（BCG）對哮喘小鼠榦細胞因子（SCF）錶達的影響。方法昆明小鼠隨機分為哮喘組、BCG組和對照組，每組10隻，以卵清蛋白（OVA）緻敏激髮建立哮喘模型。末次激髮24 h後取肺組織及支氣管肺泡灌洗液（BALF），計數嗜痠性粒細胞（EOS）；酶聯免疫吸附法檢測BALF中SCF水平；免疫組織化學圖像分析技術測定肺組織中SCF蛋白錶達。結果哮喘組、BCG組和對照組肺組織的EOS計數分彆為（10.67±1.94）箇/HP（、6.40±1.55）箇/HP和（0.37±0.33）箇/HP，BALF中EOS計數分彆為（7.58±1.30）×107/L、（3.78±1.15）×107/L和0，三組間差異有統計學意義（P均<0.01）。哮喘組、BCG組和對照組的肺組織SCF蛋白免疫組化指數分彆為（24787.97±7214.12）（、20509.50±4775.27）和（12261.66±3277.65），BALF中SCF水平分彆為（280.25±14.20）pg/ml、（266.77±31.15）pg/ml和（223.59±15.61）pg/ml，其中哮喘組和BCG組均高于對照組，差異有統計學意義（P均<0.05），BCG組與哮喘組差異無統計學意義（P>0.05）。哮喘組肺部SCF錶達與EOS計數呈正相關（P<0.05）。結論 BCG榦預能顯著減輕哮喘小鼠的氣道炎癥，但不能抑製SCF的錶達。
목적：연구잡개묘（BCG）대효천소서간세포인자（SCF）표체적영향。방법곤명소서수궤분위효천조、BCG조화대조조，매조10지，이란청단백（OVA）치민격발건립효천모형。말차격발24 h후취폐조직급지기관폐포관세액（BALF），계수기산성립세포（EOS）；매련면역흡부법검측BALF중SCF수평；면역조직화학도상분석기술측정폐조직중SCF단백표체。결과효천조、BCG조화대조조폐조직적EOS계수분별위（10.67±1.94）개/HP（、6.40±1.55）개/HP화（0.37±0.33）개/HP，BALF중EOS계수분별위（7.58±1.30）×107/L、（3.78±1.15）×107/L화0，삼조간차이유통계학의의（P균<0.01）。효천조、BCG조화대조조적폐조직SCF단백면역조화지수분별위（24787.97±7214.12）（、20509.50±4775.27）화（12261.66±3277.65），BALF중SCF수평분별위（280.25±14.20）pg/ml、（266.77±31.15）pg/ml화（223.59±15.61）pg/ml，기중효천조화BCG조균고우대조조，차이유통계학의의（P균<0.05），BCG조여효천조차이무통계학의의（P>0.05）。효천조폐부SCF표체여EOS계수정정상관（P<0.05）。결론 BCG간예능현저감경효천소서적기도염증，단불능억제SCF적표체。
Objective To study the effects of Bacillus Calmette-Guerin (BCG) intervention on the expression of stem cell factor (SCF) in asthma. Methods Kunming mice were randomly divided into asthmatic group, BCG group and control group of ten mice each group. Mice were sensitized and challenged with ovalbumin (OVA) to establish asthmatic model. After twenty-four hours of last challenge, eosinophils (EOS) were counted in the lung tissue and bronchoaveolar lavage fluid (BALF). The level of SCF in BALF was determined by enzyme-linked immunosorbent assay. The expression of SCF protein in lung tis-sue was measured by immunohistochemistry technique and computerized image analysis system. Results The number of EOS in lung tissue was (10.67±1.94)/HP, (6.40±1.55)/HP and (0.37±0.33)/HP in asthmatic, BCG and control group respectively. The number of EOS in BALF was (7.58 ± 1.30) × 107/L, (3.78 ± 1.15) × 107/L and 0 in asthmatic, BCG and control group respectively. The difference between each group was statistically significant (P<0.01). The immunohistochemical index of SCF protein in lung was (24787.97±7214.12), (20509.50±4775.27) and (12261.66±3277.65) in asthmatic, BCG and control group respectively. The SCF level of BALF was (280.25 ± 14.20) pg/ml, (266.77 ± 31.15) pg/ml and (223.59 ± 15.61) pg/ml in asthmatic, BCG and control group respectively. The SCF level in BALF in asthmatic and BCG group was significantly different from that in control group (P<0.05). There was no significant difference of SCF level in BALF between BCG and asthmatic group (P>0.05). In asth-matic group, the expression of SCF in lung was positively correlated with the number of EOS (P<0.05). Conclusions BCG treat-ment can markedly decrease the airway inflammation in asthmatic mice. BCG cannot inhibit the expression of SCF in asthma.
