Lactoferrin interacts with SPLUNC1 to attenuate lipopolysaccharide-induced inflammation of human nasal epithelial cells via down-regulated MEK1/2-MAPK signaling.
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.
a Department of Life Sciences, and Agricultural Biotechnology Center, National Chung Hsing University, Taichung 40227, Taiwan.|b Department of Otolaryngology-Head and Neck Surgery, China Medical University and Hospital, Taichung 40402, Taiwan.|c Graduate Institute of Biomedicine Sciences, China Medical University, Taichung 40402, Taiwan.
Yung-An
YA
Tsou
a Department of Life Sciences, and Agricultural Biotechnology Center, National Chung Hsing University, Taichung 40227, Taiwan.
Yu-Tong
YT
Tung
c Graduate Institute of Biomedicine Sciences, China Medical University, Taichung 40402, Taiwan.
Tsu-Fang
TF
Wu
a Department of Life Sciences, and Agricultural Biotechnology Center, National Chung Hsing University, Taichung 40227, Taiwan.
Gary Ro-Lin
GR
Chang
a Department of Life Sciences, and Agricultural Biotechnology Center, National Chung Hsing University, Taichung 40227, Taiwan.
Han-Chien
HC
Chen
b Department of Otolaryngology-Head and Neck Surgery, China Medical University and Hospital, Taichung 40402, Taiwan.|c Graduate Institute of Biomedicine Sciences, China Medical University, Taichung 40402, Taiwan.
Chia-Der
CD
Lin
d Graduate Institute of Biomedical Sciences, Chang Gung University, Taoyuan 33302, Taiwan.
Chih-Ho
CH
Lai
e Department of Bioresources, Da-Yeh University, Changhua 51591, Taiwan.
Hsiao-Ling
HL
Chen
a Department of Life Sciences, and Agricultural Biotechnology Center, National Chung Hsing University, Taichung 40227, Taiwan.|f Rong-Hsing Translational Medicine Center, iEGG Center, National Chung Hsing University, Taichung 40227, Taiwan.
Chuan-Mu
CM
Chen
D000818:Animals; D002417:Cattle; D002478:Cells, Cultured; D004847:Epithelial Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D006023:Glycoproteins / Q000378:metabolism*; D006801:Humans; D007249:Inflammation / Q000139:chemically induced / Q000378:metabolism / Q000517:prevention & control*; D007781:Lactoferrin / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000009:adverse effects*; D048369:MAP Kinase Kinase 1 / Q000378:metabolism*; D048370:MAP Kinase Kinase 2 / Q000378:metabolism*; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism*; D009297:Nasal Mucosa / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D010750:Phosphoproteins / Q000378:metabolism*; D015398:Signal Transduction
C485599:BPIFA1 protein, human; D006023:Glycoproteins; D008070:Lipopolysaccharides; D010750:Phosphoproteins; C482128:MAP2K2 protein, human; D020928:Mitogen-Activated Protein Kinases; D048369:MAP Kinase Kinase 1; D048370:MAP Kinase Kinase 2; C482125:MAP2K1 protein, human; D007781:Lactoferrin
MEK1/2; SPLUNC1; lactoferrin (LF); lactoferrine (LF); lipopolysaccharide (LPS); p42/44 MAPK