2. Academic Validation
  3. Inhibition of macrophage migration inhibitory factor alleviates LPS-induced inflammation response of HEI-OC1 cells via suppressing NF-κB signaling

Inhibition of macrophage migration inhibitory factor alleviates LPS-induced inflammation response of HEI-OC1 cells via suppressing NF-κB signaling

  • Cytokine. 2022 Feb;150:155776. doi: 10.1016/j.cyto.2021.155776.
Wenyan Zhu 1,  Wandong She 2,  Ziwen Gao 3,  Yongchi Ma 4,  Xin Jin 4
Affiliations

Affiliations

  • 1 Department of Otolaryngology-Head and Neck Surgery, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huaian, Jiangsu 223300, China. Electronic address: [email protected].
  • 2 Department of Otolaryngology-Head and Neck Surgery, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, Nanjing, Jiangsu 210008, China.
  • 3 Department of Otorhinolaryngology, Head and Neck Surgery, Lower Saxony Center for Biomedical Engineering, Implant Research and Development (NIFE), Hannover Medical School, Stadtfelddamm 34, 30625 Hannover, Germany.
  • 4 Department of Otolaryngology-Head and Neck Surgery, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huaian, Jiangsu 223300, China.
PMID: 34864396 DOI: 10.1016/j.cyto.2021.155776
Abstract

Background: Sudden sensorineural hearing loss (SSNHL) is acute and unexplained. Macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine in several inflammatory diseases. However, its role in SSNHL remains elusive.

Methods: Lipopolysaccharide (LPS) was used to induce the inflammatory response of murine auditory cells, HEI-OC1. Silencing of MIF in HEI-OC1 cells was achieved by transfection of short hairpin RNA against MIF. 740Y-P and IMD0354 were used to stimulate the PI3K pathway and suppress the NF-κB pathway, respectively. RT-qPCR and western blotting were used to examine MIF and cyclooxygenase 2 (COX2) expression in LPS-treated HEI-OC1 cells. ELISA was employed to assess prostaglandin E2 (PGE2) concentrations.

Results: MIF was upregulated in LPS-treated HEI-OC1 cells. MIF knockdown reduced PGE2 synthesis and COX2 expression in LPS-treated HEI-OC1 cells. Moreover, MIF knockdown suppressed activation of the PI3K/Akt and NF-κB pathway in LPS-treated HEI-OC1 cells. Additionally, inhibition of MIF decreased PGE2 production and COX2 expression via inactivation of the NF-κB pathway.

Conclusion: Inhibition of MIF alleviated LPS-induced inflammation in HEI-OC1 cells via inactivating the NF-κB signaling, which might provide a better understanding for SSNHL development.

Keywords

COX2; MIF; NF-κB signaling; PGE2; SSNHL.

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