Effect of Cholesterol Depletion on Interleukin-8 Production in Human Respiratory Epithelial Cells.
10.4168/aair.2013.5.6.402
- Author:
Min Jung KIM
1
;
Jung Yeon HONG
;
Kyung Eun LEE
;
Kyung Won KIM
;
Myung Hyun SOHN
;
Kyu Earn KIM
Author Information
1. Department of Pediatrics and Institute of Allergy, Severance Medical Research Institute, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea. kekim@yuhs.ac
- Publication Type:Original Article
- Keywords:
Cholesterol;
epithelial cell;
inflammation;
interleukin-8;
MAP kinase signaling system
- MeSH:
beta-Cyclodextrins;
Butadienes;
Cell Membrane;
Cholesterol;
Enzyme-Linked Immunosorbent Assay;
Epithelial Cells;
Humans;
Immune System;
Inflammation;
Inflammation Mediators;
Interleukin-8;
Interleukins;
MAP Kinase Signaling System;
Nitriles;
p38 Mitogen-Activated Protein Kinases;
Phosphotransferases;
Protein Kinases
- From:Allergy, Asthma & Immunology Research
2013;5(6):402-408
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: The lipid entities of cell membranes are components of the immune system and important mediators of inflammation. Despite increasing interest in the function of epithelial cells in inflammation, the role of cholesterol in this process has not been described. Here, we investigated the effect of cholesterol depletion on the inflammatory process in airway epithelial cells via the expression of interleukin (IL)-8 as a marker of inflammation. METHODS: A 549 cells were treated with 0.5% methyl-beta-cyclodextrin as a selective cholesterol extractor. The IL-8 level was assessed by enzyme-linked immunosorbent assay and reassessed after cholesterol repletion. Mitogen-activated protein kinase (MAPK) inhibitors were used to determine the upstream signaling pathway for IL-8 production in cholesterol-depleted cells. RESULTS: We found a relationship between the amount of cholesterol in A 549 cells and inflammation of the airway. IL-8 production was increased in cholesterol-depleted A 549 cells and restored by cholesterol repletion. IL-8 production was decreased by pretreatment with the extracellular signal-regulated kinase (ERK) inhibitor U0126 but not with JNK inhibitor II or the p38 MAPK inhibitor SB202190. CONCLUSIONS: Our findings suggest that inflammatory responses are increased in cholesterol-depleted epithelial cells via the MAPK signaling system, predominantly by the ERK pathway. We conclude that the lipid components of airwayepithelial cells may play a role in the inflammatory process.
