Xuesong Li1, *, Peipei Li2, Yujie Wu2, Shi Wang3, Chundong Xu3


1Shanghai Public Health Clinical Center, Shanghai 201514, PR China - 2Hefei BOE Hospital, Hefei 230012, PR China - 3Funing People's Hospital, Yancheng 224400, PR China


Objective: To explore the mechanism by which 15 lipoxygenase 1 (15lo1) regulates the synthesis of chemokine ligand 26 (CCL26) by activating the extracellular signal regulated kinase (ERK) pathway in nasal polyp (NP) epithelial cells.

Methods: 45 cases of nasal polyps in our hospital from January 2018 to June 2019 were selected as the nasal polyp group, and 25 normal nasal mucosa samples were selected as the control group. The middle turbinate (MT) and inferior turbinate (IT) epithelial cells, and nasal polyp and middle turbinate epithelial cells in the nasal polyp group, were extracted and compared for 15 LO1 mRNA and protein expression levels. Some nasal polyp epithelial cells were randomly divided into a control group and an IL-3 group. The control group was not treated with any treatment. The IL-3 group was stimulated with IL-13 for 5 days. The mRNA and protein expression levels of 15lo1 and CCL26 in the control group and the IL-13 group were compared at 1-5 days, and the correlation between them was also observed; ALOX15 was used in the nasal polyp group. The expression level of 15lo1 was knocked down by siRNA transfection, in which the control group was transfected with scrambles siRNA, and the expression level of 15lo1 protein in each group was further compared; two ERK signal pathway blockers, PD98059 and U0126, were used to treat the epithelial cells of the control group and the nasal polyp group, and the protein expression levels of t-ERK, p-ERK and CCL26 in each group were compared.

Results: The expression levels of 15lo1 protein and mRNA in epithelial cells of the nasal polyp group were significantly higher than those of the control group (P<0.05). The expression levels of 15lo1, CCL26 protein and mRNA in the IL-3 group were significantly higher than those in the control group on 1D, 3D and 5D, and showed a time-dependent manner (P<0.05). There was a significant positive correlation between 15lo1 and CCL26 gene expression (r=0.720, P=0.003), and there was a moderate positive correlation between 15lo1 and CCL26 protein expression (r=0.600, P=0.012). The expression of CCL26 protein in the ALOX15 siRNA group was significantly lower than that in the control group (P<0.05). The protein levels of p-ERK and CCL26 in the U0126 group and the PD98059 group were significantly higher than those in the nasal polyp group (P<0.05).

Conclusion: The expression level of 15lo1 in nasal polyp epithelial cells is significantly increased, and this can regulate the synthesis of CCL26 by regulating the activation of the ERK signaling pathway, which may become a new target for the treatment of nasal polyps.


Nasal polyps, 15lo1, ERK, CCL26.