Abstract: Objective To investigate the effects of LPS on inflammation and mucus hypersecretion in the airway of asthmatic mice. Methods Thirty clean BALB/c mice were randomly divided into three groups: asthmatic model group (AST group, n=10), LPS+asthmatic group (LAS group,n=10), control group (NS group, n=10). Mice in the asthmatic model group were sensitized and challenged with ovalbumin (OVA). Mice in the LPS group were not only sensitized and challenged with OVA but also inhaled LPS. Mice in the control group were sensitized and challenged with normal sodium. Total cells and differential inflammatory cells in bronchoalveolar lavage fluid (BALF) were counted. The levels of IL-4 and TNF-α in BALF were determined by ELISA. Pathomorphological changes in the lungs were observed by hematoxylin-eosin (HE) staining. Goblet cells of the airway walls were observed by AB-PAS staining. The expression of Mucin-5ac (Muc5ac) in airway were determined by immunohistochemical staining. The expressions of Muc5ac mRNA in lung tissues were determined by real time fluorescence quantitative reverse transcription polymerase (real time-PCR). Results Mice in the LAS and AST groups had more total cells and eosinophil, monocytes and lymphocyte cells in BALF, higher levels of IL-4 and TNF-α in BALF, greater hyperplasia of goblet cells in the airway walls, and higher levels of expression of Muc5ac in lung tissues than those in the control group (P<0.05). Mice in the LAS group had higher levels of airway inflammation and airway mucus hypersecretion in lung tissues than those in the AST group (P<0.05). Conclusion OVA stimulates lymphocyte and eosinophil cells in the airway inflammation of asthmatic mice. Goblet cell metaplasia and airway mucus hypersecretion are obvious in asthmatic mice. Higher levels of airway inflammation and mucus hypersecretion in lung tissues can be found in mice inhaled LAS compared with those in the AST group. LAS may stimulate inflammatory mediators.