The Soluble Tumor Necrosis Factor-Alpha Receptor Suppresses Airway Inflammation in a Murine Model of Acute Asthma.
10.3349/ymj.2009.50.4.569
- Author:
Hae Seong NAM
1
;
Sook Young LEE
;
Seung Jun KIM
;
Ju Sang KIM
;
Soon Seog KWON
;
Young Kyoon KIM
;
Kwan Hyung KIM
;
Hwa Sik MOON
;
Jeong Sup SONG
;
Sung Hak PARK
;
Seok Chan KIM
Author Information
1. Division of Pulmonology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea. cmcksc@catholic.ac.kr
- Publication Type:Original Article
- Keywords:
Asthma;
soluble TNF-alpha receptor;
airway inflammation
- MeSH:
Animals;
Anti-Asthmatic Agents/*therapeutic use;
Asthma/*drug therapy/*immunology;
Blotting, Western;
Bronchi/drug effects;
Bronchial Hyperreactivity;
Bronchoalveolar Lavage Fluid/immunology;
Enzyme-Linked Immunosorbent Assay;
Female;
Immunohistochemistry;
Inflammation/*drug therapy;
Interleukin-13/metabolism;
Interleukin-4/metabolism;
Interleukin-5/metabolism;
Mice;
Mice, Inbred BALB C;
Ovalbumin/pharmacology;
Tumor Necrosis Factor-alpha/*therapeutic use
- From:Yonsei Medical Journal
2009;50(4):569-575
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Tumor necrosis factor-alpha (TNF-alpha) is a proinflammatory cytokine that has been implicated in many aspects of the airway pathology in asthma. TNF-alpha blocking strategies are now being tried in asthma patients. This study investigated whether TNF-alpha blocking therapy inhibits airway inflammation and airway hyperresponsiveness (AHR) in a mouse model of asthma. We also evaluated the effect of TNF-alpha blocking therapy on cytokine production and adhesion molecule expression. MATERIALS AND METHODS: Ovalbumin (OVA) sensitized BALB/c female mice were exposed to intranasal OVA administration on days 31, 33, 35, and 37. Mice were treated intraperitoneally with soluble TNF-alpha receptor (sTNFR) during the OVA challenge. RESULTS: There were statistically significant decreases in the numbers of total cell and eosinophil in bronchoalveolar lavage fluid (BALF) in the sTNFR treated group compared with the OVA group. However, sTNFR-treatment did not significantly decrease AHR. Anti-inflammatory effect of sTNFR was accompanied with reduction of T helper 2 cytokine levels including interleukin (IL)-4, IL-5 and IL-13 in BALF and vascular cell adhesion molecule 1 expression in lung tissue. CONCLUSION: These results suggest that sTNFR treatment can suppress the airway inflammation via regulation of Th2 cytokine production and adhesion molecule expression in bronchial asthma.
