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

• Published in: PloS one 2015-12, Vol.10 (12), p.e0143484-e0143484
• Main Authors: Tsou, Yung-An, Lin, Chia-Der, Chen, Hui-Chen, Hsu, Hui-Ying, Wu, Lii-Tzu, Chiang-Ni, Chuan, Chen, Chih-Jung, Wu, Tsu-Fang, Kao, Min-Chuan, Chen, Yu-An, Peng, Ming-Te, Tsai, Ming-Hsui, Chen, Chuan-Mu, Lai, Chih-Ho
• Format: Article
• Language: English
• Subjects: Activation; Allergies; Analysis; Antimicrobial activity; Antimicrobial agents; Attenuation; Bacteria; Bacteria - isolation & purification; Bacterial infections; Biofilms; c-Jun protein; Care and treatment; Cell Line, Tumor; Colonization; Complications and side effects; Cytokines; Disease; Epithelial cells; Epithelium; Gene expression; Genetic aspects; Glycoproteins - genetics; Health aspects; Helper cells; Hospitals; Humans; Immunoglobulins; Immunology; Infections; Influence; Interleukin; Interleukin 13; Interleukin-13 - pharmacology; Interleukins; Leukocytes (eosinophilic); Life sciences; Lipopolysaccharides; Lipopolysaccharides - pharmacology; Lungs; Lymphocytes T; MAP Kinase Kinase 4 - metabolism; Medicine; Nasal Mucosa - cytology; Nasal Mucosa - drug effects; Nasal Mucosa - metabolism; Nasal Mucosa - microbiology; Otolaryngology; Palate; Patients; Permeability; Phosphoproteins - genetics; Polyps; Protein expression; Proteins; Proto-Oncogene Proteins c-jun - metabolism; Pseudomonas; Respiratory tract; Rhinosinusitis; Rodents; Signal transduction; Signaling; Sinuses; Surfactants; Surgery; Transcription factors; Up-Regulation
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0143484

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.