Objective  To analyze the immune characteristics of short-term chronic obstructive pulmonary disease (COPD) model induced by peptide challenge after smoking exposure. Methods  A short-term murine model of COPD was established by smoking sensitization and peptide infusion challenge. Airway inflammation was analyzed by histological staining sections of lung tissues and cells of bronchoalveolar lavage fluid. An invasive lung function test was used to measure changes of lung respiratory mechanical parameters in experimental mice.The Luminex instrument platform was employed to quantify concentrations of cytokines in lung homogenates. Flow cytometry was used to measure changes in the numbers and proportions of subsets of T helper (Th) cells  and innate lymphoid cells (ILCs) in mouse lung tissues. Results  The data showed that short-term tobacco smoke exposure and peptide challenge caused damage of the alveoli, induced airways inflammation with neutrophil infiltration, increased the expression of type 3 cytokines and the numbers of Th17 and ILC3, while decreased proportion of ILC1 and ILC2. Conclusion  The short-term COPD models of smoke sensitization and peptide challenge are dominated by type 3 immunity, in which ILC3 may play a more important role than Th17.