Lactoferrin interacts with SPLUNC1 to attenuate lipopolysaccharide-induced inflammation of human nasal epithelial cells via down-regulated MEK1/2-MAPK signaling

Yung An Tsou, Yu Tong Tung, Tsu Fang Wu, Gary Ro Lin Chang, Han Chien Chen, Chia Der Lin, Chih Ho Lai, Hsiao Ling Chen, Chuan Mu Chen

Research output: Contribution to journalArticle

7 Citations (Scopus)

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 languageEnglish
Pages (from-to)394-399
Number of pages6
JournalBiochemistry and Cell Biology
Volume95
Issue number3
DOIs
Publication statusPublished - 2017
Externally publishedYes

Keywords

  • Lactoferrin (LF)
  • Lipopolysaccharide (LPS)
  • MEK1/2
  • P42/44 MAPK
  • SPLUNC1

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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