Abstract
The short palate, lung, and nasal epithelium clone 1 (SPLUNC1) protein is an important innate material in the upper airway, and lactoferrin (LF) aids the innate functions in humans. In this study, a nasal epithelial model was used to investigate how LF modulates SPLUNC1 to reduce the inflammatory process mediated by lipopolysaccharide (LPS). The inflammation of human RPMI-2650 cells was induced with LPS to evaluate SPLUNC1 expression after treating the cells with bovine LF (bLF). The interaction pathway between LF and SPLUNC1 in LPS-induced inflammation was further investigated. Our study reveals that the addition of bLF results in the recovery of SPLUNC1 expression in nasal epithelial cells under LPS-induced inflammation. MAPK is involved in the main pathway for the SPLUNC1 and bLF interaction. Decreased SPLUNC1 function could be recovered by addition of bLF. The MEK1/2-MAPK signaling pathway is crucial for the SPLUNC1 and bLF interaction. Therefore, LF could support SPLUNC1 in the innate immunity recovery process.
Original language | English |
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Pages (from-to) | 394-399 |
Number of pages | 6 |
Journal | Biochemistry and Cell Biology |
Volume | 95 |
Issue number | 3 |
DOIs | |
Publication status | Published - 2017 |
Externally published | Yes |
Keywords
- Lactoferrin (LF)
- Lipopolysaccharide (LPS)
- MEK1/2
- P42/44 MAPK
- SPLUNC1
ASJC Scopus subject areas
- Biochemistry
- Molecular Biology
- Cell Biology