Distribution of IL-4, IL-8 and GM-CSF in Nasal Turbinate Mucosa Following Sulfur Dioxide Exposure In Vitro.
- Author:
Chul Hee LEE
1
;
Kang Soo LEE
;
Chae Seo RHEE
;
Byeong Ho SONG
Author Information
1. Department of Otorhinolaryngology, College of Medicine, Seoul National University, Seoul, Korea. chulhee@plaza.snu.ac.kr
- Publication Type:In Vitro ; Original Article
- Keywords:
Sulfur dioxide;
IL-4;
IL-8;
GM-CSF;
Nasal epithelium
- MeSH:
Air Pollutants;
Colony-Stimulating Factors;
Cytokines;
Epithelial Cells;
Epithelium;
Granulocyte-Macrophage Colony-Stimulating Factor*;
Humans;
Inflammation;
Interleukin-4*;
Interleukin-8*;
Mucous Membrane*;
Nasal Mucosa;
Sulfur Dioxide*;
Sulfur*;
Turbinates*
- From:Journal of Rhinology
1999;6(1):19-23
- CountryRepublic of Korea
- Language:English
-
Abstract:
There is increasing evidence that airway epithelial cells, when exposed to various gas-derived air pollutants, play an important role in airway inflammation by releasing inflammatory cytokines. However, there is little information on air pollutant-induced cytokine expression at the tissue level and on the role of sulfur dioxide (SO2), one of the major ambient air pollutants, in cytokine production. We studied whether or not a low concentration of sulfur dioxide induces an increase in tissue expression of interleukin-4 (IL-4), interleukin-8 (IL-8), and granulocyte/macrophage colony stimulating factor (GM-CSF). After exposing surgically obtained normal human nasal turbinates to 0.05 ppm SO2 for one hour, we conducted specific immunohistochemical staining to assess the tissue expression of each cytokine. We found that the percent expression of IL-8 and GM-CSF in the surface epithelium was significantly higher in each SO2-exposed tissue than in the matched control tissue. However, there was no significant difference in the number of submucosal IL-4-positive cells between exposed and control specimens. These results suggest that exposure to a low concentration of SO2 increases airway inflammation, apparently by inducing an increase in the expression of GM-CSF and IL-8.
