Eotaxin和CCR3在哮喘豚鼠肺和骨髓组织的表达及调控

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目的:通过观察哮喘豚鼠肺和骨髓组织Eotaxin/CCR3表达的变化及糖皮质激素对其影响,探讨哮喘及激素干预的可能机制。方法:用卵白蛋白(OVA)致敏法制备豚鼠哮喘模型,分为正常对照组、哮喘组和激素干预(治疗组)组,瑞氏染色计数骨髓涂片和外周血涂片中白细胞比例,免疫组织化学技术检测骨髓中CCR3的表达;制备豚鼠肺组织病理标本,苏木精-伊红染色,原位分子杂交技术检测肺组织中Eotaxin mRNA,免疫组织化学技术检测Eotaxin在肺组织中的表达。结果:哮喘组骨髓涂片及外周血涂片中嗜酸粒细胞(EOS)比例显著高于对照组及治疗组(P<0.01);与对照组比较,哮喘组肺组织中Eotaxin阳性细胞数与Eotaxin mRNA表达明显增强(P<0.01),且两者呈正相关性(r=0.804,P<0.01)。哮喘组肺组织Eotaxin的表达与EOS的数量呈显著正相关(r=0.795,P<0.01)。哮喘组骨髓涂片中CCR3阳性细胞比例显著高于对照组及治疗组(P<0.01),哮喘组骨髓涂片中CCR3阳性细胞比例和外周血EOS比例呈显著正相关(r=0.736,P<0.05),治疗组与哮喘组比较骨髓中CCR3阳性细胞的比例有显著性下降(P<0.05),但仍高于对照组(P<0.05)。结论:哮喘豚鼠肺组织中Eotaxin和骨髓CCR3表达增强,为EOS从骨髓快速募集到肺组织提供了可能,激素通过下调肺组织Eotaxin及骨髓CCR3的表达,发挥抗EOS性气道炎症的作用。 OBJECTIVE: To investigate the changes of Eotaxin / CCR3 expression in lung and bone marrow of asthmatic guinea pigs and the effects of glucocorticoid on the possible mechanism of asthma and hormone intervention. Methods: Guinea pig asthma model was established by ovalbumin (OVA) sensitization method and divided into normal control group, asthma group and hormone intervention group (treatment group), Wright’s staining count bone marrow smear and peripheral blood smear in leukocyte ratio, immunization Histochemistry was used to detect the expression of CCR3 in the bone marrow. The lung tissues of guinea pigs were prepared for histopathology. Eotaxin mRNA was detected by hematoxylin-eosin staining and in situ hybridization in situ hybridization. The expression of Eotaxin in lung tissue was detected by immunohistochemistry. Results: The percentage of eosinophils (EOS) in bone marrow smear and peripheral blood smear in asthma group was significantly higher than that in control group and treatment group (P <0.01). Compared with control group, the number of Eotaxin positive cells in asthmatic group Eotaxin mRNA expression was significantly increased (P <0.01), and the two were positively correlated (r = 0.804, P <0.01). There was a significant positive correlation between Eotaxin expression and the number of EOS in the asthmatic group (r = 0.795, P <0.01). The percentage of CCR3-positive cells in asthma group was significantly higher than that in control group and treatment group (P <0.01). There was a significant positive correlation between the proportion of CCR3 positive cells in peripheral blood and bone marrow smear in asthma group (r = 0.736, P < 0.05). The ratio of CCR3 positive cells in bone marrow of the treatment group and the asthma group was significantly lower than that of the control group (P <0.05), but still higher than that of the control group (P <0.05). Conclusion: The expression of Eotaxin and bone marrow CCR3 in lung tissue of asthmatic guinea pigs is enhanced, which makes it possible for EOS to rapidly recruite to the lung tissue from the bone marrow. Hormone exerts anti-EOS airway inflammation by down-regulating the expression of Eotaxin and bone marrow CCR3.
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