肺炎支原体感染伴喘息患儿免疫功能变化的研究

Study of immunologic function of children with mycoplasma pneumoniae infection associated with asthma

目的探讨肺炎支原体感染伴喘息患儿的细胞及体液免疫功能的变化。方法选择2012年1~12月在我院治疗的肺炎支原体感染伴喘息患儿30例,和在我院进行治疗肺炎支原体感染不伴喘息的患儿30例,比较两组细胞免疫及体液免疫相关指标改变。结果研究组CD3＋为61.9±10.4、CD3＋CD8＋为22.7±6.9、CD19＋为23.9±3.7,显著低于对照组（P〈0.05或〈0.01）。而CD3＋CD4＋、CD4/CD8、CD16＋CD56＋两组比较差异无统计学意义（P〉0.05）。研究组IgA为0.9±0.2,显著低于对照组（P〈0.05）。两组IgM、IgG比较差异无统计学意义（P〉0.05）。结论肺炎支原体感染后,通过刺激气道上皮慢性炎症、直接损伤呼吸道上皮细胞,导致气道高反应性,从而诱发喘鸣。

Objective To discuss immunologic function of children with mycoplasma pneumoniae infection associated with asthma. Methods 30 cases with mycoplasma pneumoniae infection associated with asthma, and 30 cases with mycoplasma pneumoniae infection without asthma were selected. Cellular immunity and humoral immunity of two groups were compared. Results CD3＋（61.9±10.4）,CD3＋CD8＋（22.7±6.9）,CD19＋（23.9±3.7）of study group were lower than that of control group（P＆lt;0.05 or P＆lt;0.01）. CD3＋CD4＋ ,CD4/CD8,CD16＋CD56＋ of two groups had no significant difference （P＆gt;0.05）. IgA （0.9±0.2） of study group was lower than that of control group （P＆lt;0.05）. IgM, IgG of two groups had no significant difference （P＆gt;0.05）. Conclusion Mycoplasma pneumoniae infection leads to airway hyperresponsiveness, inducing stridor, by stimulating the airway epithelium chronic inflammation, directly damaging to respiratory epithelial cells.