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Published on: April 2, 2014
DMBT1 Alleviates Nasal Airway Inflammatory Response in the LPS-Induced Nasal Polyp Model
Xiaoqing Lu1, He Xu2, Liang Shan1
1Department of Otorhinolaryngology & Head and Neck Surgery, Shanghai Fourth People's Hospital Affiliated to Tongji University School of Medicine, Shanghai, China.
Introduction:
The aim of this study was to investigate the effects and mechanism of deleted in malignant brain tumors 1 (DMBT1) protein on the mouse model of nasal polyps.
Methods:
The mouse model of nasal polyps was induced by intranasal drip intervention of lipopolysaccharide (LPS) 3 times a week for 12 weeks. A total of 42 mice were randomly divided into blank group, LPS group, and LPS+DMBT1 group. DMBT1 protein was applied by intranasal drip intervention in each nostril after LPS. After 12 weeks, 5 mice in each group were randomly picked for the mouse olfactory disorder experiment, 3 mice were randomly picked for histopathological observation of nasal mucosa, 3 mice for olfactory marker protein (OMP) immunofluorescence analysis and the last 3 mice were grabbed for nasal lavage, and the levels of cytokines interleukin (IL)-4, IL-5, IL-13, and phosphatidylinositide 3-kinases (PI3K) in the nasal lavage fluid were detected by enzyme-linked immunosorbent assay (ELISA).
Results:
Compared with the blank group, mice in LPS group had olfactory dysfunction, the level of OMP was significantly reduced, the nasal mucosa was swollen, discontinuous, and contained a large number of inflammatory cells. The levels of IL-4, IL-5, IL-13, and PI3K in the nasal lavage fluid were significantly increased in LPS group (p < 0.01). Compared with the LPS group, the number of mice with olfactory dysfunction in the LPS+DMBT1 group was less, the infiltration of inflammatory cells was reduced, the OMP-positive cells were significantly increased, and the IL-4, IL-5, IL-13, and PI3K in the nasal lavage fluid were significantly increased, p < 0.01.
Conclusions:
DMBT1 protein alleviates the nasal airway inflammatory response in the mouse nasal polyp model, and the mechanism may be through the PI3K-AKT signaling pathway.
