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Updated: Jan 4, 2026
Culturing of Human Nasal Epithelial Cells at the Air Liquid Interface
Published on: October 8, 2013
Fipronil upregulates inflammatory cytokines and MUC5AC expression in human nasal epithelial cells
1Department of Medical Science, College of Medicine, Graduate School of Yeungnam University, Daegu, Republic of Korea; Department of Otorhinolaryngology-Head and Neck Surgery, College of Medicine, Yeungnam University, Daegu, Republic of Korea.
Background:
Airway inflammation and excessive mucin production are pathophysiological characteristics of airway diseases. Fipronil, a pesticide, is being extensively used in agriculture and veterinary medicine worldwide. However, this compound impairs immune function in non-target organisms. The present study aimed to evaluate the effect of fipronil on pro-inflammatory cytokine and mucus production and signalling pathways in human primary nasal METHODOLOGY: The effect of fipronil on pro-inflammatory cytokine and MUC5AC expression and the signalling pathway of fipronil were investigated using real-time PCR, enzyme immunoassays, immunofluorescence, and immunoblot analysis with specific inhibitors and small interfering RNA.
Results:
Fipronil treatment increased pro-inflammatory cytokine interleukin (IL)-1beta, IL-6, IL-8, and MUC5AC expression in human primary nasal epithelial cells. It also induced phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) mitogenactivated protein kinase (MAPK), p38 MAPK, and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB). MAPK and NF-kB inhibitor treatment significantly inhibited increases in IL-1beta, IL-6, IL-8, and MUC5AC expression. Ex vivo data confirmed that fipronil-induced MUC5AC expression occurs through ERK1/2, p38, and NF-kB signalling pathways in nasal inferior turbinate tissue.
Conclusions:
Fipronil induced pro-inflammatory cytokine IL-1beta, IL-6, IL-8, and MUC5AC expression via ERK1/2 MAPK, p38 MAPK, and NF-kB in human primary nasal epithelial cells.
Insights
The pesticide fipronil increases airway inflammation by boosting pro-inflammatory cytokines and MUC5AC expression. This occurs through the extracellular signal-regulated kinase 1/2 (ERK1/2) mitogen-activated protein kinase (MAPK), p38 MAPK, and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) pathways.
Area of Science:
- Immunology
- Toxicology
- Cell Biology
Background:
- Airway inflammation and excessive mucus are hallmarks of respiratory diseases.
- Fipronil, a widely used pesticide, can compromise immune function in non-target organisms.
- Understanding fipronil's impact on airway cells is crucial for public health.
Purpose of the Study:
- To investigate the effects of fipronil on pro-inflammatory cytokine and MUC5AC (mucus) production in human nasal cells.
- To elucidate the specific signaling pathways involved in fipronil-induced airway responses.
Main Methods:
- Human primary nasal epithelial cells and ex vivo nasal tissue were utilized.
- Real-time PCR, enzyme immunoassays, immunofluorescence, and immunoblot analysis were performed.
- Specific inhibitors and small interfering RNA were employed to dissect signaling pathways.
Main Results:
- Fipronil significantly increased the expression of interleukin (IL)-1beta, IL-6, IL-8, and MUC5AC in nasal cells.
- Fipronil induced the activation of extracellular signal-regulated kinase 1/2 (ERK1/2) mitogen-activated protein kinase (MAPK), p38 MAPK, and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB).
- Inhibiting MAPK and NF-kB pathways significantly reduced fipronil-induced cytokine and MUC5AC production, confirming their role.
Conclusions:
- Fipronil exposure stimulates pro-inflammatory cytokine and MUC5AC expression in human nasal epithelial cells.
- These effects are mediated through the activation of ERK1/2 MAPK, p38 MAPK, and NF-kB signaling pathways.
- The findings highlight fipronil as a potential contributor to airway inflammation and mucus hypersecretion.
