中国医药导刊
中國醫藥導刊
중국의약도간
CHINESE JOURNAL OF MEDICAL GUIDE
2014年
11期
1387-1388,1390
,共3页
陈金海%姚明%卞晓琴%张金蓉
陳金海%姚明%卞曉琴%張金蓉
진금해%요명%변효금%장금용
肺炎支原体%支气管哮喘%小儿%免疫%抗体
肺炎支原體%支氣管哮喘%小兒%免疫%抗體
폐염지원체%지기관효천%소인%면역%항체
Mycoplasma pneumoniae%Bronchial asthma%Child%Immune%Antibody
目的：探讨肺炎支原体（MP）感染与儿童支气管哮喘的相关性。方法：将住院治疗的100例支气管哮喘急性发作期患儿作为哮喘组，另选100例同期至本院儿科诊治的上呼吸道感染患儿作为上感组，再选50例至我院体检的健康儿童作为对照组。比较三组患儿MP-IgM滴度以及MP-IgM阳性率；将哮喘组患儿分为MP-IgM阳性组（MP+组）和MP-IgM阴性组（MP-组），比较这两组与对照组患儿之间血清总免疫球蛋白E（总IgE）、外周血嗜酸性粒细胞（EOS）绝对值、白介素-2（IL-2）、IL-4、干扰素-γ（IFN-γ）、血清可溶性白介素-2受体（sIL-2R）、肿瘤坏死因子-α（TNF-α）以及超氧化物歧化酶（SOD）水平。结果：①哮喘组MP-IgM滴度和阳性率均显著高于上感组和对照组（P＜0.01）。②MP+组和MP-组血清总IgE和外周血EOS绝对值均显著高于对照组，MP+组亦显著高于MP-组（P＜0.01）；MP+组和MP-组血清IL-2、IFN-γ和SOD水平均显著低于对照组，IL-4、sIL-2R和TNF-α显著高于对照组（P＜0.01），MP+组和MP-组之间亦有显著差异（P＜0.01）。结论：MP感染是诱发或加重小儿支气管哮喘的重要因素之一，它可以通过破坏Th1/Th2的动态平衡，激发气道急慢性炎症，最终引起免疫机制紊乱而致病。
目的：探討肺炎支原體（MP）感染與兒童支氣管哮喘的相關性。方法：將住院治療的100例支氣管哮喘急性髮作期患兒作為哮喘組，另選100例同期至本院兒科診治的上呼吸道感染患兒作為上感組，再選50例至我院體檢的健康兒童作為對照組。比較三組患兒MP-IgM滴度以及MP-IgM暘性率；將哮喘組患兒分為MP-IgM暘性組（MP+組）和MP-IgM陰性組（MP-組），比較這兩組與對照組患兒之間血清總免疫毬蛋白E（總IgE）、外週血嗜痠性粒細胞（EOS）絕對值、白介素-2（IL-2）、IL-4、榦擾素-γ（IFN-γ）、血清可溶性白介素-2受體（sIL-2R）、腫瘤壞死因子-α（TNF-α）以及超氧化物歧化酶（SOD）水平。結果：①哮喘組MP-IgM滴度和暘性率均顯著高于上感組和對照組（P＜0.01）。②MP+組和MP-組血清總IgE和外週血EOS絕對值均顯著高于對照組，MP+組亦顯著高于MP-組（P＜0.01）；MP+組和MP-組血清IL-2、IFN-γ和SOD水平均顯著低于對照組，IL-4、sIL-2R和TNF-α顯著高于對照組（P＜0.01），MP+組和MP-組之間亦有顯著差異（P＜0.01）。結論：MP感染是誘髮或加重小兒支氣管哮喘的重要因素之一，它可以通過破壞Th1/Th2的動態平衡，激髮氣道急慢性炎癥，最終引起免疫機製紊亂而緻病。
목적：탐토폐염지원체（MP）감염여인동지기관효천적상관성。방법：장주원치료적100례지기관효천급성발작기환인작위효천조，령선100례동기지본원인과진치적상호흡도감염환인작위상감조，재선50례지아원체검적건강인동작위대조조。비교삼조환인MP-IgM적도이급MP-IgM양성솔；장효천조환인분위MP-IgM양성조（MP+조）화MP-IgM음성조（MP-조），비교저량조여대조조환인지간혈청총면역구단백E（총IgE）、외주혈기산성립세포（EOS）절대치、백개소-2（IL-2）、IL-4、간우소-γ（IFN-γ）、혈청가용성백개소-2수체（sIL-2R）、종류배사인자-α（TNF-α）이급초양화물기화매（SOD）수평。결과：①효천조MP-IgM적도화양성솔균현저고우상감조화대조조（P＜0.01）。②MP+조화MP-조혈청총IgE화외주혈EOS절대치균현저고우대조조，MP+조역현저고우MP-조（P＜0.01）；MP+조화MP-조혈청IL-2、IFN-γ화SOD수평균현저저우대조조，IL-4、sIL-2R화TNF-α현저고우대조조（P＜0.01），MP+조화MP-조지간역유현저차이（P＜0.01）。결론：MP감염시유발혹가중소인지기관효천적중요인소지일，타가이통과파배Th1/Th2적동태평형，격발기도급만성염증，최종인기면역궤제문란이치병。
[ABSTRACT]Objective:To explore the relation between mycoplasma pneumoniae infection and bronchial asthma in children. Methods:One hundred cases of children on acute attack of asthma acted as asthma group. 100 cases of children with upper respiratory infection at the same term acted as URI group. Another 50 cases of healthy children with physical examination acted as control group. The titer and positive incidence of MP-IgM among three groups were compared. The children in asthma group were divided into MP-IgM positive group (MP+group) and MP-IgM negative group (MP-group). The levels of total serum immunoglobulin E (total IgE), peripheral acidophilic granulocyte (EOS) absolute value, interleukin-2 (IL-2), IL-4, interferon-γ(IFN-γ), serum soluble interleukin 2 receptor (sIL-2R), tumor necrosis factor-α(TNF-α) and superoxide dismutase (SOD) among these two groups and control group were compared. Results:①The titer and positive incidence of MP-IgM in asthma group were signiifcantly higher than that in URI group and control group (P<0.01).②The levels of total IgE and EOS absolute value in MP+group and MP-group were signiifcantly higher than that in control group, and the lMP+group were signiifcantly higher than that in MP-group (P<0.01). The levels of serum IL-2, IFN-γand SOD in MP+group and MP-group were signiifcantly lower than that in control group, while the levels of IL-4, sIL-2R and TNF-αwere signiifcantly higher than that in control group (P<0.01). There were also signicant differences between MP+group and MP-group (P<0.01). Conclusions:MP infection is one important factor of inducing or aggravating asthma in children. It may break Th1/Th2 dynamic balance, increase acute&chronic respiratory tract inlfammation, so as to cause immune dysfunction.
