The effect of rhinovirus and cigarette smoke extract on the production of interleukin-8 in human bronchial epithelial cells.
- Author:
Young Chan KIM
1
;
Jae Hyung LEE
;
Mi Ok KIM
;
Tae Hyung KIM
;
Jang Won SOHN
;
Ho Joo YOON
;
Dong Ho SHIN
;
Sung Soo PARK
Author Information
1. Department of Internal Medicine, Hanyang University College of Medicine, Seoul, Korea. hjyoon@hanyang.ac.kr
- Publication Type:In Vitro ; Original Article
- Keywords:
Rhinovirus;
Cigarette;
IL-8;
Asthma;
COPD
- MeSH:
Asthma;
Enzyme-Linked Immunosorbent Assay;
Epithelial Cells*;
Humans*;
Interleukin-8*;
Interleukins;
Precipitating Factors;
Pulmonary Disease, Chronic Obstructive;
Respiratory System;
Rhinovirus*;
RNA, Messenger;
Smoke*;
Smoking;
Tobacco Products*
- From:Korean Journal of Medicine
2005;69(6):660-667
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Rhinovirus (RV) or smoking are one of the most important precipitating factors in acute exacerbation of COPD and bronchial asthma. We hypothesized that alterations in interleukin (IL)-8 elaboration are present at sites of RV infection and cigarette smoke stimulation and also there is an additive effect if both agents are present in bronchial epithelial cells. To test this hypothesis, we characterized time-sequenced alterations in IL-8 elaboration from human bronchial epithelial cells in vitro under the stimuli of RV and cigarette smoke extract (CSE). METHODS: We compared the ability of RV-infected and/or CSE-stimulated bronchial epithelial cells, BEAS-2B (from American Type Culture Collection) cells to produce the IL-8 with controls. We stimulated BEAS-2B cells with RV 14 and/or CSE. We harvest the supernatants from RV and/or CSE- stimulated BEAS-2B cells and the controls at 2 hr, 4 hr, 6 hr, 12 hr, 24 hr, 48 hr from inoculation time. We measured the concentration of IL-8 by ELISA kits from supernatants and analysed IL-8 mRNA transcript semiquantitatively by RT-PCR. RESULTS: RV-infected and/or CSE-stimulated BEAS-2B cells increased the production of IL-8 from 24hr and produced outstandingly compared with the controls at 48 hr and there were an additive effects when both agents were present, especially in the combinations of RV and CSE stimuli. CONCLUSIONS: Our results demonstrate that RV infection and components of cigarette smoke elicit inflammatory responses in bronchial epithelial cells and RV and CSE could be more harmful to respiratory tract in combination.
