Effect of Resolvin D1 and E1 on Mucin Expression in Human Airway Epithelial Cells.
10.3342/kjorl-hns.2018.00164
- Author:
Hyung Geun KIM
1
;
Tae Yeong CHOI
;
Chang Hoon BAE
;
Yoon Seok CHOI
;
Hyung Gyun NA
;
Si Youn SONG
;
Yong Dae KIM
Author Information
1. Department of Otorhinolaryngology-Head and Neck Surgery, College of Medicine, Yeungnam University, Daegu, Korea. ydkim@med.yu.ac.kr
- Publication Type:Original Article
- Keywords:
Human airway epithelial cells;
MUC4;
MUC5AC;
MUC5B;
Resolvin
- MeSH:
B-Lymphocytes;
Blotting, Western;
Enzyme-Linked Immunosorbent Assay;
Epithelial Cells*;
Humans*;
Lubrication;
Methods;
Mortality;
Mucins*;
Mucus;
p38 Mitogen-Activated Protein Kinases;
Phosphorylation;
Phosphotransferases;
Protein Kinases;
RNA, Messenger
- From:Korean Journal of Otolaryngology - Head and Neck Surgery
2019;62(1):28-35
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND AND OBJECTIVES: Mucin is an important component of mucus that performs the first line of defense against inhaled pathogens and particles, lubrication of organs, and protection of airway. It is hyper-secreted in inflammatory airway diseases and is associated with morbidity and mortality of the affected patients. Resolvin, an autacoid of a specific lipid structure, exhibits anti-inflammatory property against inflammatory airway diseases although its effects on mucin secretion by human airway epithelial cells have not yet been demonstrated. In this regard, we investigated the effects of Resolvin on lipopolysaccharide (LPS)-induced mucin expression in human airway epithelial cells. MATERIALS AND METHOD: In mucin-producing human NCI-H292 epithelial cells, the effects and brief signaling pathways of Resolvin D1 (RvD1) and Resolvin E1 (RvE1) on the LPS-induced MUC4, MUC5AC, and MUC5B expression were investigated using reverse transcription-polymerase chain reaction, enzyme-linked immunosorbent assay and Western blot analysis. RESULTS: RvD1 attenuated LPS-induced MUC4, MUC5AC, and MUC5B mRNA expression and protein production in human NCI-H292 cells while RvE1 did not. RvD1 significantly blocked LPS-induced activated phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) mitogen-activated protein kinase (MAPK) and p38 MAPK and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) while RvE1 did not. CONCLUSION: These results suggest that RvD1 attenuates LPS-induced MUC4, MUC5AC, and MUC5B expressions via ERK1/2 MAPK, p38 MAPK, and NF-κB signaling pathways in airway epithelial cells. Therefore, RvD1 may modulate the control of mucus-hypersecretion in inflammatory airway diseases.
