Interleukin-13 Inhibits Lipopolysaccharide- Induced BPIFA1 Expression in Nasal Epithelial Cells

Yung An Tsou, Chia Der Lin, Hui Chen Chen, Hui Ying Hsu, Lii Tzu Wu, Chuan Chiang-Ni, Chih Jung Chen, Tsu Fang Wu, Min Chuan Kao, Yu An Chen, Ming Te Peng, Ming Hsui Tsai, Chuan Mu Chen, Chih Ho Lai

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8 Scopus citations


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 LPSinduced 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.

Original languageEnglish
Article numbere0143484
JournalPLoS ONE
Issue number12
StatePublished - 01 12 2015

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© 2015 Tsou et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in anymedium, provided the original author and source are credited.


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