［ABSTRACT］ Objective: The murine model of atopic march was established by percutaneous sensitization with MC903 combined with papain, followed by intranasal challenge with papain to induce airway inflammation. Methods: The murine model of atopic march was established by percutaneous sensitization with MC903 combined with papain, followed by intranasal challenge with papain to induce airway inflammation. The murine model was evaluated from different aspects, including histopathology of skin and lung tissues, quantitative expression of immuno-inflammatory molecules, inflammatory cell counting in bronchoalveolar lavage fluid (BALF) and lung tissues. In addition, whole-transcriptome sequencing of immune cells in lung tissues and functional analysis of differentially expressed genes were performed. Results: Compared with the control group, the ear skin of mice in the atopic march model group was significantly thickened. Histopathological examination showed obvious acanthosis and mast cell infiltration, and the expression of IL-4 was significantly upregulated. In the lung tissue pathology of model mice, significant peribronchial inflammatory cell infiltration and increased mucus secretion by bronchial epithelial goblet cells were observed. The numbers of eosinophils and neutrophils in bronchoalveolar lavage fluid and lung tissue were significantly increased, and the expressions of IL-4 and IL-17A cytokines in lung tissue were significantly upregulated. Whole-transcriptome sequencing of lung tissue immune cells indicated that pathways such as eosinophil and neutrophil chemotaxis, and inflammatory response were significantly activated in the model group mice. Conclusions: Percutaneous sensitization with papain combined with MC903 followed by intranasal challenge with papain can induce a murine model of atopic march dominated by Th2 and Th17 airway inflammation. This model exhibits an airway inflammation phenotype with mixed infiltration of eosinophils and neutrophils, providing a new animal model for the study of mixed granulocytic asthma.