目的：探讨红霉素对哮喘豚鼠气道炎症的影响。方法：以卵蛋白(OVA)致敏的过敏性哮喘豚鼠为模型,诱喘后24 h取支气管肺泡灌洗液(BALF)进行细胞分类及右肺中叶HE染色,镜下观察支气管肺组织形态学改变并对BALF及气道壁嗜酸粒细胞、中性粒细胞、单核细胞进行计数。结果：哮喘组BALF及支气管管壁嗜酸粒细胞、中性粒细胞、单核细胞数分别为:[B3ALF(10.9±1.2)×108/L,(3.9±0.7)×108/L,(4.2±1.0)×108/L:支气管管壁(73.6±8.8)个/HP,(7.1±1.9)个/HP,(3.5±0.7)个/HP],分别与正常对照组比较[BALF(0.5±0.1)×108/L,(0.4±0.1)×108/L,(2.0±0.4)×108/L;支气管管壁(5.5±1.6)个/HP,(1.2±0.9)个/HP,(0.7±0.5)个/HP],均显著增高(P<0.01或0.05),红霉素组BALF及支气管管壁嗜酸粒细胞、中性粒细胞、单核细胞数分别为[BALF(3.3±0.5)×108/L,(1.7±0.2)×108/L,(3.1±0.7)×108/L;支气管管壁(38.7±5.6)个/HP,(3.7±0.8)个/HP,(2.2±1.0)个/HP],较哮喘组明显下降(P<0.01或0.05),但较正常对照组仍显著增加(P<0.01或0.05)。结论：红霉素能减轻哮喘豚鼠气道炎症反应,具有抗炎作用,但红霉素不能完全阻断这种气道炎症反应。

OBJECTIVE: To study the effect of erythromycin on airway inflammation in asthmatic guinea pigs. METHODS: A model of allergic asthma was developed by sensitizing guinea pigs with ovalbumin. Twenty - four hours after the induction of asthma, cells in bronchoalveolar lavage fluid (BALF) were categorized, the right lung was processed for histopathological examination and the numbers of eosinophils, neuthrophils and monocytes in the BALF and bronchial lumen were counted. Eight normal guinea pigs were used as the controls. RESULTS: The numbers of eosinophils, neuthrophils and monocytes in the BALF [(10.9 ± 1.2), (3.9 ± 0.7) and (4.2 ± 1.0) × 108/L, respectively] and bronchial lumen [(73.6 ±8. 8), (7.1 ± 1.9) and (3.5 ± 0.7) high powered field (HP), respectively] of the asthma group were significantly higher compared to those in the BALF [(0.5 ±0.1), (0.4±0.1) and (2.0 ± 0.4) × 108/L, respectively] and bronchial lumen [(5.5 ±1.6), (1.2 ± 0.9) and (0.7±0.5)/HP, respectively] of the controls ( P< 0.01 or 0.05). After pretreatment with erythromycin, eosinophils neutrophils, and monocytes in the BALF [(3.3 ± 0.5), (1.710.2) and (3.1 ±0.7) × 108/L, respectively] and bronchial lumen [(38.7 ± 5.6), (3.7±0.8) and (2.2 ±1.0)/HP, respectively] of the asthma group decreased significantly ( P <0.01 or 0.05), but remained higher than those of the controls. CONCLUSIONS: Erythromycin alleviates but does not block completely airway inflammatory reactivity.