Objective To investigate the variation of mice BALF IL-4、IL-12 and IL-13 in different periods from senrnsitized to challenged ,of asthmatic model, and further explored the immunological pathogenesis mechanism of asthma.rnMethods The model of asthma in mice was established by egg protein sensitizing 55BalB/C mice were randomly dividrned into eleven groups included 1 control group(N), and each group contains five mice. Four sensitized groups werernnamed S(Ⅰ-Ⅳ)which were divided by the four phases of sensitizing and six challenged groups were named C(Ⅰ-Ⅳ)rnwhich were divided by the six phases of challenging. All sensitized and challenged groups were administered intraperitornneally 0.1 ml of 0.01% OVA and 0. lml of 20% AI(OH)3. The four phases of sensitized was divided into four groups,rnthe sensitized group Ⅰ was injected twice and the group Ⅱ third, group Ⅲ fourth and group Ⅳ was injected fifth.rnThen the challenged groups were continue accepted with 5%OVA aerosol inhaling after being sensitized. OVA aerosolrninhaling was lasting 27 days, the six phases of challenged was selected the 7 d,ll d,15 d,19 d,23 d and 27 d respecrntively. The normal control group was injected and inhalated saline instead of OVA. The levels of BALF IL-4, IL-12 andrnIL-13 of each group were measured by ELISA kit. Results The BALF IL-4 and IL-13 levels of challenged mice werernhigher than that of sensitized, however the IL-12 level of challenged mice was lower than the sensitized mice. We alsornfound that the IL-4 and IL-13 levels were gradually raised along with the increased frequency of OVA inhalation, whilernthe IL-12 level decreased. For the stimulated group,the IL-12 level was significantly degraded from SI group, while thernIL-4 and IL-13 levels were significantly elevated from SII group. IL-4 and IL-13 showed a significantly positive correlarntion (r=0. 968), IL-12 and IL-4 were negative correlated (r=-0. 771), IL-12 and IL-13 were significantly negativerncorrelated(r= -0. 856). Conclusion IL-12 was initially degraded during the sensitization of mice. With further stimurnlation,IL-13 was started to elevate,and accompanied with the inflammatory cells proliferating and infiltrating into thernlungs,the IL-4 level was gradually elevated. We concluded that these different cytokines take part in the occurrence andrndevelopment of asthma in different phases, which are important to study the immunological pathogenesis of asthma.%目的 研究细胞因子IL-4、IL-12、IL-13在哮喘小鼠模型致敏和激发的不同时期的浓度变化,进一步探究哮喘的免疫学发病机制.方法 以卵白蛋白致敏法制备小鼠哮喘模型,将55只BalB/C小鼠按随机数字表法分为11组,每组5只,即正常对照组(N)、刺激(S)I-Ⅳ组、激发(C)Ⅰ-Ⅵ组.所有小鼠均予0.01%卵白蛋白(OVA)和2%Al(OH)3 各0.1 ml腹腔注射以致敏,注射两次者为刺激Ⅰ组,三次者为刺激Ⅱ组,四次者为刺激Ⅲ组,五次者为刺激Ⅳ组.激发组小鼠在刺激五次后予5%OVA雾化吸入,连续吸入激发7 d者为激发Ⅰ组,11 d者为激发Ⅱ组,15 d者为激发Ⅲ组,19 d者为激发Ⅳ组,23 d者为激发Ⅴ组,27 d者为激发Ⅵ组.正常对照组以生理盐水代替OVA进行腹腔注射和雾化吸入.用ELISA方法检测各组小鼠肺泡灌洗液中IL-4、IL-12、IL-13浓度.结果 激发组小鼠肺泡灌洗液IL-4和IL-13水平比刺激组高,IL-12水平比刺激组低,且随雾化吸入5%OVA的激发次数增加,IL-4、IL-13水平逐渐升高,IL-12水平逐渐降低.刺激组小鼠,IL-12水平从刺激Ⅰ组开始明显降低,IL-13和IL-4水平从刺激Ⅱ组开始明显升高.IL-4与IL-13呈显著正相关(r=0.968),IL-12与IL-4显著负相关(r＝-0.771),IL-12与IL-13显著负相关(r=-0.856).结论 IL-12水平在致敏过程中首先降低.随着继续刺激,IL-13水平开始显著增高,并伴随炎症细胞在肺部浸润增多,IL-4水平缓慢增高.这些细胞因子在哮喘的发生发展过程中各自起到了不同的作用,从而为研究哮喘的免疫学发病机制奠定了基础.
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