The Soluble Tumor Necrosis Factor-Alpha Receptor Suppresses Airway Inflammation in a Murine Model of Acute Asthma

• Published in: Yonsei medical journal Vol. 50; no. 4; pp. 569 - 575
• Main Authors: Nam, Hae-Seong, Lee, Sook Young, Kim, Seung Jun, Kim, Ju Sang, Kwon, Soon Seog, Kim, Young Kyoon, Kim, Kwan Hyung, Moon, Hwa Sik, Song, Jeong Sup, Park, Sung Hak, Kim, Seok Chan
• Format: Journal Article
• Language: English
• Published: Korea (South) Yonsei University College of Medicine 31.08.2009; 연세대학교의과대학
• Subjects: Animals; Anti-Asthmatic Agents - therapeutic use; Asthma - drug therapy; Asthma - 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; Original; Ovalbumin - pharmacology; Tumor Necrosis Factor-alpha - therapeutic use; 의학일반; airway inflammation; soluble TNF-α receptor; Asthma
• ISSN: 0513-5796; 1976-2437; 1976-2437
• DOI: 10.3349/ymj.2009.50.4.569

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. 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. 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. These results suggest that sTNFR treatment can suppress the airway inflammation via regulation of Th2 cytokine production and adhesion molecule expression in bronchial asthma.