室内燃煤PM2.5对卵蛋白诱导哮喘大鼠的气道炎症作用

Effect of PM2.5 from coal combustion indoor on airway inflammation in the asthmtic rats induced by ovalbumin

目的:探讨室内燃煤PM2.5对卵蛋白(OVA)诱导哮喘大鼠的气道炎症作用及其对肺组织病理改变。方法:将40只6周龄雄性SD大鼠随机分为Control、OVA、PM2.5、PM2.5+OVA 4组,通过气管滴注分别予以生理盐水、OVA(15μg/mL)和(或)PM2.5(2.5 mg/mL)混悬液200μL,2周/次,共4次。末次染毒24 h后收集支气管肺泡灌洗液(Balf)检测炎性细胞的分布、白介素4(IL-4)、γ干扰素(IFN-γ),右上肺组织做HE染色及电镜切片。结果:PM2.5+OVA组炎性细胞较Control组增多(P<0.05),主要以淋巴细胞及单核细胞为主;HE染色镜下见Control组炎性细胞浸润较少,PM2.5组及OVA组炎性细胞中等量浸润,PM2.5+OVA组大量炎性细胞浸润;电镜下Control组未见异常,OVA组可见有大量即将脱落细胞,局部可见II型细胞破损,PM2.5组可见内皮细胞广泛水肿,肺泡间隔可见大量纤维,PM2.5+OVA组炎性细胞浸润,细胞器大量破坏,基底膜厚度不均,气血屏障结构不清晰;PM2.5+OVA组IL-4与Control组、OVA组及PM2.5组间均有差异(P<0.05),IFN-γPM2.5+OVA组较Control组有差异(P<0.05),IL-4与IFN-γ呈负相关(r=-0.358,P<0.05)。结论:室内燃煤PM2.5加重OVA诱导的哮喘大鼠气道炎性细胞浸润及病理性改变。

Objective To investigate the effect of indoor coal PM2.5 on the airway inflammation and the pathological morphology alterations of lung tissue in asthmatic rats induced by ovalbumin （OVA）. Methods Forty six-week-old male SD rats were randomly divided into four groups （Control, OVA, PM2.5, PM2.5 ＋ OVA）. Normal saline, OVA （15μg/mL） and （or） PM2.5 （2.5 mg/ mL） were given to rats in the four groups through intratracheal instillation for four times （two weeks one time） , respectively. Twenty- four hours after the last intratracheal instillation, bronchoalveolar irrigation lavage fluid （BALF） was collected for determinations of serum interleukin 4 （IL-4）, interferon gamma （IFN-γ）. The lung tissue was collected for HE staining and electron microscopy detection. Results HE staining showed less inflammatory cell infiltration was observed in the control group; In PM2.5 group and OVA group, there was medium quantity of inflammatory cell infiltration, In PM2.5 ＋ OVA group, severe inflammatory cell infiltration was observed. Electron microscopy showed no abnormal lung tissue in the control group, but organelles were gradually destroyed, endothelial cell edama, alveolar interval with a large number of fibersin were observed in PM2.5 group. The exfoliated cells, local type II cells with visible damage were found in OVA group. A large number of fibers were existed among the lung tissues and organelles were destroyed, thickness of basement membrane was non- uniform, and blood air barrier structure was not clear in PM2.5 ＋ OVA group. Compared with PM2.5 ＋ OVA group, concentration of IL-4 in PM2.5, OVA and the control group was siganificantly different （P 〈 0.05）. A negative correlation between IL-4 and IFN-γ was observed （r =-0.358, P 〈 0.05）. Conclusion Indoor coal PM2.5 exacerbates the airway inflammatory cell infiltration and airway remodeling in OVA-induced asthmatic rats.