Related Experiment Video
Updated: Mar 29, 2026
Intra-tracheal Administration of Haemophilus influenzae in Mouse Models to Study Airway Inflammation
Published on: March 2, 2016
Interleukin-13 Inhibits Lipopolysaccharide-Induced BPIFA1 Expression in Nasal Epithelial Cells
Yung-An Tsou1,2, Chia-Der Lin1,3, Hui-Chen Chen3
1Department of Otolaryngology-Head and Neck Surgery, China Medical University and Hospital, Taichung, Taiwan.
Insights
Interleukin 13 (IL-13) suppresses bactericidal/permeability-increasing fold containing family A, member 1 (BPIFA1) expression in nasal cells via the JNK/c-Jun pathway. This mechanism contributes to bacterial infections in chronic rhinosinusitis with nasal polyps.
Area of Science:
- Immunology
- Molecular Biology
- Respiratory Medicine
Background:
- Bactericidal/permeability-increasing fold containing family A, member 1 (BPIFA1), formerly SPLUNC1, exhibits antimicrobial properties and is expressed in airway epithelium.
- Reduced BPIFA1 expression correlates with bacterial colonization in chronic rhinosinusitis with nasal polyps (CRSwNP).
- Interleukin 13 (IL-13) is implicated in airway allergies and suppresses BPIFA1 expression, but its precise mechanism in bacterial infections is unknown.
Purpose of the Study:
- To elucidate the molecular mechanism by which IL-13 affects bacterial infection and BPIFA1 expression in the respiratory tract.
- To investigate the role of the JNK/c-Jun signaling pathway in regulating BPIFA1 expression.
Main Methods:
- Investigated lipopolysaccharide (LPS)-induced BPIFA1 expression in nasal epithelial cells.
- Utilized Western blotting to assess the activation of the JNK/c-Jun signaling pathway.
- Performed immunohistochemical analysis on patient samples.
Main Results:
- LPS-induced BPIFA1 expression is mediated by JNK/c-Jun pathway activation and AP-1.
- IL-13 inhibits LPS-induced JNK and c-Jun phosphorylation, subsequently reducing BPIFA1 expression.
- Immunohistochemistry revealed IL-13 suppresses BPIFA1 in eosinophilic CRSwNP patients with bacterial infections.
Conclusions:
- IL-13 significantly attenuates bacteria-induced BPIFA1 expression through the JNK/c-Jun pathway.
- This IL-13-mediated suppression of BPIFA1 may contribute to the pathogenesis of eosinophilic CRSwNP.
- Understanding this pathway offers potential therapeutic targets for CRSwNP.
Abstract:
Short palate, lung, and nasal epithelium clone 1 (SPLUNC1) protein is expressed in human nasopharyngeal and respiratory epithelium and has demonstrated antimicrobial activity. SPLUNC1 is now referred to as bactericidal/permeability-increasing fold containing family A, member 1 (BPIFA1). Reduced BPIFA1 expression is associated with bacterial colonization in patients with chronic rhinosinusitis with nasal polyps (CRSwNP). Interleukin 13 (IL-13), predominately secreted by T helper 2 (TH2) cells, has been found to contribute to airway allergies and suppress BPIFA1 expression in nasal epithelial cells. However, the molecular mechanism of IL-13 perturbation of bacterial infection and BPIFA1 expression in host airways remains unclear. In this study, we found that lipopolysaccharide (LPS)-induced BPIFA1 expression in nasal epithelial cells was mediated through the JNK/c-Jun signaling pathway and AP-1 activation. We further demonstrated that IL-13 downregulated the LPS-induced activation of phosphorylated JNK and c-Jun, followed by attenuation of BPIFA1 expression. Moreover, the immunohistochemical analysis showed that IL-13 prominently suppressed BPIFA1 expression in eosinophilic CRSwNP patients with bacterial infection. Taken together, these results suggest that IL-13 plays a critical role in attenuation of bacteria-induced BPIFA1 expression that may result in eosinophilic CRSwNP.
