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目的探讨IL-23、IL-17在支气管哮喘发病中的作用。方法将30只健康雌性BALB/c小鼠随机分为3组:分别为卵白蛋白(OVA)致敏并激发的哮喘模型组(A组),OVA致敏、激发并予糖皮质激素治疗组(B组)及正常对照组(C组),每组10只。末次激发24h后,各组小鼠摘眼球取血,ELISA法检测其血清IL-17、IFN-γ和IL-23水平。收集支气管肺泡灌洗液(BALF),行嗜酸性粒细胞(EOS)计数。HE染色观察其肺组织病理改变。RT-PCR法检测其肺组织IL-17mRNA、IL-23mRNA表达。结果 1.B组多数小鼠未见明显行为学异常反应,肺组织病理损害也较A组明显减轻,BALF中EOS计数[(16.4±1.7)×107L-1]亦显著低于A组[(45.5±2.1)×107L-1](P<0.01)。2.A组小鼠血清IL-17、IL-23水平[(94.42±3.41)ng.L-1,(155.56±12.50)ng.L-1]均高于C组[(41.76±2.07)ng.L-1,(51.49±6.34)ng.L-1],IFN-γ水平[(20.91±1.59)ng.L-1]低于C组[(53.23±1.74)ng.L-1],其差异均有统计学意义(Pa<0.01);且IL-23与IL-17水平呈正相关(r=0.763,P<0.05),IL-23、IL-17与IFN-γ均无相关性。而B组小鼠血清IL-17、IL-23水平[(56.01±3.92)ng.L-1,(88.00±6.43)ng.L-1]均低于A组,IFN-γ水平[(31.66±1.29)ng.L-1]高于A组,其差异均有统计学意义(Pa<0.01)。3.A组小鼠肺组织IL-17mRNA、IL-23mRNA的表达均高于C组(Pa<0.01),且IL-23mRNA与IL-17mRNA表达量呈正相关(r=0.628,P<0.05);而B组小鼠肺组织IL-17mRNA、IL-23mRNA的水平均低于A组(Pa<0.01)。A组肺组织IL-17mRNA表达量与BALF中EOS计数呈正相关(r=0.849,P<0.01),IL-23mRNA表达量与BALF中EOS计数无相关性。结论 IL-17、IL-23参与哮喘大鼠的发病,IL-17可能与哮喘EOS增多有关,IL-23可能是通过诱导IL-17的产生间接促进哮喘发病,糖皮质激素对其有抑制作用。
Objective To investigate the role of IL-23 and IL-17 in the pathogenesis of bronchial asthma. Methods Thirty healthy female BALB / c mice were randomly divided into three groups: model group (group A) sensitized and challenged with ovalbumin (OVA), sensitized with OVA, and challenged with glucocorticoid treatment group B group) and normal control group (C group), 10 rats in each group. After the last challenge, the mice in each group were sacrificed and the serum levels of IL-17, IFN-γ and IL-23 were measured by ELISA. Bronchoalveolar lavage fluid (BALF) was collected for eosinophil count (EOS). The pathological changes of lung tissue were observed by HE staining. The expression of IL-17 mRNA and IL-23 mRNA in lung tissue was detected by RT-PCR. Results 1. Most mice in group B showed no significant behavioral abnormalities and pathological lesions in lung tissue were also significantly reduced compared with those in group A. The count of EOS in BALF [(16.4 ± 1.7) × 107L-1] was also significantly lower than that in group A [( 45.5 ± 2.1) × 107L-1] (P <0.01). The level of IL-17 and IL-23 in group A was significantly higher than that in group C [(94.42 ± 3.41) ng.L-1, (155.56 ± 12.50) ng.L-1] [(41.76 ± 2.07) ng (51.49 ± 6.34) ng.L-1], and IFN-γ levels in patients with chronic hepatitis B were significantly lower than those in patients in C group [(20.91 ± 1.59) ng.L-1] (P <0.01). There was a positive correlation between IL-23 and IL-17 (r = 0.763, P <0.05). There was no correlation between IL-23, IL-17 and IFN-γ. The levels of IL-17 and IL-23 in group B were significantly lower than those in group A [(56.01 ± 3.92) ng.L-1, (88.00 ± 6.43) ng.L-1] [(31.66 ± 1.29) ng.L-1] were higher than those in A group (P <0.01). The expression of IL-17mRNA and IL-23mRNA in lung tissue of mice in group A was higher than that in group C (P <0.01), and there was a positive correlation between IL-23mRNA and IL-17mRNA (r = 0.628, However, the levels of IL-17 mRNA and IL-23 mRNA in lungs of group B were lower than those in group A (P <0.01). There was a positive correlation between the level of IL-17mRNA in BALF and the count of EOS in BALF in group A (r = 0.849, P <0.01). There was no correlation between the level of IL-23mRNA and the count of EOS in BALF. Conclusion IL-17 and IL-23 are involved in the pathogenesis of asthma in rats. IL-17 may be related to the increase of EOS in asthma. IL-23 may indirectly contribute to the pathogenesis of asthma by inducing the production of IL-17, which may be inhibited by glucocorticoid .