ArticleYonsei medical journal2009
The soluble tumor necrosis factor-alpha receptor suppresses airway inflammation in a murine model of acute asthma.
Article in Yonsei medical journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 27 citations in OpenAlex.
- Inflammation in Asthma: Mechanistic Insights and the Role of Biologics in Therapeutic Frontiers.Biomedicines · 2025Review
- The interplay of DAMPs, TLR4, and proinflammatory cytokines in pulmonary fibrosis.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Clinicopathologic and Transcriptomic Analysis of Radiation-Induced Lung Injury in Nonhuman Primates.International journal of radiation oncology, biology, physics · 2021Article
- Zinc and iron complexes of oleanolic acid, (OA) attenuate allergic airway inflammation in rats.Inflammopharmacology · 2019Article
- The EGFR-ADAM17 Axis in Chronic Obstructive Pulmonary Disease and Cystic Fibrosis Lung Pathology.Mediators of inflammation · 2018Review
- Migratory eosinophilic alveolitis caused by radiation therapy.Journal of thoracic disease · 2015Article
- CFTR Gene Mutations and Asthma in Indian Children: A Case-Control Study.Indian journal of clinical biochemistry : IJCB · 2015Article
- Effect of aging on airway remodeling and muscarinic receptors in a murine acute asthma model.Clinical interventions in aging · 2013Article
- Association between cystic fibrosis transmembrane conductance regulator gene mutations and susceptibility for childhood asthma in Korea.Yonsei medical journal · 2010Article
- Protective Effect of S-Allyl Cysteine Against Neonatal Asthmatic Rats.Dose-response : a publication of International Hormesis SocietyArticle
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTumor 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
methodsOvalbumin (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.
resultsThere 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.
conclusionThese results suggest that sTNFR treatment can suppress the airway inflammation via regulation of Th2 cytokine production and adhesion molecule expression in bronchial asthma.
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