Establishment of a mouse model of lipopolysaccharide‑induced neutrophilic nasal polyps

Wang,Shuibin; Zhang,Hanwu; Xi,Zulian; Huang,Jingjing; Nie,Jun; Zhou,Bin; Deng,Yuqin; Tao,Zezhang

doi:10.3892/etm.2017.5208

Establishment of a mouse model of lipopolysaccharide‑induced neutrophilic nasal polyps

Authors:
- Shuibin Wang
- Hanwu Zhang
- Zulian Xi
- Jingjing Huang
- Jun Nie
- Bin Zhou
- Yuqin Deng
- Zezhang Tao
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Affiliations: Department of Otolaryngology‑Head and Neck Surgery, Yichang Yiling Hospital, Yichang, Hubei 443100, P.R. China, Department of Otolaryngology‑Head and Neck Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China
Published online on: September 27, 2017 https://doi.org/10.3892/etm.2017.5208
Pages: 5275-5282
Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Research has identified that gram‑negative bacteria have an important role in refractory nasal polyps. In the present study, lipopolysaccharide (LPS) was used to establish a mouse model with neutrophilic nasal polyps in order to explore the effect and mechanism of LPS on the formation of neutrophilic nasal polyps in mice. A total of 5 or 10 µg of LPS was dropped into the nasal cavities of C57BL/6J mice in order to establish animal models with neutrophilic nasal polyps. Histological staining, toll‑like receptor 4 (TLR4), cluster of differentiation 68 for macrophages and myeloperoxidase for neutrophil immunohistochemistry were used to observe histopathological changes in the nasal mucosa. The expression levels of cytokines, including interferon (IFN)‑γ, tumor necrosis factor (TNF)‑α, interleukin (IL)‑4 and IL‑17 in the nasal lavage fluid, were detected by ELISA. Compared with the control group, mice in the LPS groups exhibited significant mucosa epithelial cell damage and nasal polyp formation. Furthermore, TLR4+ cells, macrophages, neutrophils and significantly increased levels of IFN‑γ, TNF‑α, and IL‑17 in the nasal lavage fluids were indicated (all P=0.008). These findings indicated that LPS is able to activate the TLR4 receptor pathway to induce the formation of neutrophilic nasal polyps in mice. Additionally, LPS administration was accompanied by a significant increase in the number of macrophages, T helper (Th) 1 and Th17‑related cytokines (P=0.009, P=0.008 and P=0.008, respectively). Therefore, the present model is commensurate with the characteristics of primary nasal polyps that have been identified in the Asian population.

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