The pathological changes in the airway induced by the co-treatment were more remarkable than B. adusta treatment alone, suggesting that H-ASD enhances B.adusta-induced lung eosinophilia via remarkable increases of these pro-inflammatory mediators, especially eosinophil-relevant chemokine MCP-3, cytokine IL-5 and Th2-mediated cytokine IL-13. The gene discussed is IL5; the disease is medical procedure.