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- Title
The Soluble Tumor Necrosis Factor-Alpha Receptor Suppresses Airway Inflammation in a Murine Model of Acute Asthma.
- Authors
Hae-Seong Nam; 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
- Abstract
Purpose: Tumor necrosis factor-alpha (TNF-α) is a proinflammatory cytokine that has been implicated in many aspects of the airway pathology in asthma. TNF-α blocking strategies are now being tried in asthma patients. This study investigated whether TNF-α blocking therapy inhibits airway inflammation and airway hyperresponsiveness (AHR) in a mouse model of asthma. We also evaluated the effect of TNF-α blocking therapy on cytokine production and adhesion molecule expression. Meterials 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-α 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.
- Subjects
ASTHMA; INFLAMMATION; OBSTRUCTIVE lung diseases; TUMOR necrosis factors; GLYCOPROTEINS; CYTOKINES
- Publication
Yonsei Medical Journal, 2009, Vol 50, Issue 4, p569
- ISSN
0513-5796
- Publication type
Article
- DOI
10.3349/ymj.2009.50.4.569