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- Publisher Website: 10.1046/j.1365-2222.2003.01615.x
- Scopus: eid_2-s2.0-0037338372
- PMID: 12614451
- WOS: WOS:000181330600016
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Article: Anti-inflammatory effects of high-dose montelukast in an animal model of acute asthma
Title | Anti-inflammatory effects of high-dose montelukast in an animal model of acute asthma |
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Authors | |
Keywords | Eotaxin IgE Interleukin-13 Interleukin-4 Interleukin-5 Leukotrienes VCAM-1 |
Issue Date | 2003 |
Publisher | Blackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CEA |
Citation | Clinical and experimental allergy, 2003, v. 33 n. 3, p. 359-366 How to Cite? |
Abstract | Background Asthmatic inflammation is mediated by a network of cytokines, chemokines and adhesion molecules. Corticosteroids are the only effective agents available to control asthmatic inflammation. We investigated the effect of high-dose montelukast (MK), a selective cysteinyl leukotriene receptor 1 antagonist, on mediators of airway inflammation.
Objective The aim of this study was to determine the effect of a 3-day course of high-dose MK on mediators of airway inflammation induced by a single allergen challenge in sensitized mice.
Methods Ovalbumin (OVA)-sensitized BALB/c mice were treated with 25 mg/kg of MK or saline intravenously for 3 days. On the third day, a single inhalation challenge with OVA was given. Cellular infiltration was assessed in the bronchoalveolar lavage (BAL) and in the lung. Expression of IL-4, IL-5, IL-13 and eotaxin in the BAL, and the lung was determined. Serum IL-5 and total IgE was measured. IL-5 and eotaxin mRNA expression in the lung was determined. Finally, eotaxin and VACM-1 expression in the lung was assessed by immunohistochemistry.
Results MK reduced the number of eosinophils in the BAL by > 90%. There was also significant reduction in IL-5 in the BAL, lung and the serum, and IL-5 mRNA expression in the lung. IL-4 level in the lung and BAL, and IL-13 level in the lung also significantly decreased. Serum IgE level and lung VCAM-1 expression was also significantly lower in treated animals, but eotaxin protein and mRNA expression in the lung remained unchanged.
Conclusion MK exerts its anti-inflammatory effect through the suppression of T helper type-2 (Th2) cytokines. The use of high-dose MK as an anti-inflammatory agent in acute asthma should be further explored. |
Persistent Identifier | http://hdl.handle.net/10722/222900 |
ISSN | 2023 Impact Factor: 6.3 2023 SCImago Journal Rankings: 1.290 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Wu, AY | - |
dc.contributor.author | Chik, SC | - |
dc.contributor.author | Chan, AW | - |
dc.contributor.author | Li, Z | - |
dc.contributor.author | Tsang, KW | - |
dc.contributor.author | Li, W | - |
dc.date.accessioned | 2016-02-12T01:25:33Z | - |
dc.date.available | 2016-02-12T01:25:33Z | - |
dc.date.issued | 2003 | - |
dc.identifier.citation | Clinical and experimental allergy, 2003, v. 33 n. 3, p. 359-366 | - |
dc.identifier.issn | 0954-7894 | - |
dc.identifier.uri | http://hdl.handle.net/10722/222900 | - |
dc.description.abstract | Background Asthmatic inflammation is mediated by a network of cytokines, chemokines and adhesion molecules. Corticosteroids are the only effective agents available to control asthmatic inflammation. We investigated the effect of high-dose montelukast (MK), a selective cysteinyl leukotriene receptor 1 antagonist, on mediators of airway inflammation. Objective The aim of this study was to determine the effect of a 3-day course of high-dose MK on mediators of airway inflammation induced by a single allergen challenge in sensitized mice. Methods Ovalbumin (OVA)-sensitized BALB/c mice were treated with 25 mg/kg of MK or saline intravenously for 3 days. On the third day, a single inhalation challenge with OVA was given. Cellular infiltration was assessed in the bronchoalveolar lavage (BAL) and in the lung. Expression of IL-4, IL-5, IL-13 and eotaxin in the BAL, and the lung was determined. Serum IL-5 and total IgE was measured. IL-5 and eotaxin mRNA expression in the lung was determined. Finally, eotaxin and VACM-1 expression in the lung was assessed by immunohistochemistry. Results MK reduced the number of eosinophils in the BAL by > 90%. There was also significant reduction in IL-5 in the BAL, lung and the serum, and IL-5 mRNA expression in the lung. IL-4 level in the lung and BAL, and IL-13 level in the lung also significantly decreased. Serum IgE level and lung VCAM-1 expression was also significantly lower in treated animals, but eotaxin protein and mRNA expression in the lung remained unchanged. Conclusion MK exerts its anti-inflammatory effect through the suppression of T helper type-2 (Th2) cytokines. The use of high-dose MK as an anti-inflammatory agent in acute asthma should be further explored. | - |
dc.language | eng | - |
dc.publisher | Blackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CEA | - |
dc.relation.ispartof | Clinical and experimental allergy | - |
dc.rights | The definitive version is available at www.blackwell-synergy.com | - |
dc.subject | Eotaxin | - |
dc.subject | IgE | - |
dc.subject | Interleukin-13 | - |
dc.subject | Interleukin-4 | - |
dc.subject | Interleukin-5 | - |
dc.subject | Leukotrienes | - |
dc.subject | VCAM-1 | - |
dc.subject.mesh | Acetates - administration & dosage - pharmacokinetics | - |
dc.subject.mesh | Asthma - drug therapy | - |
dc.subject.mesh | Chemokines, CC - genetics | - |
dc.subject.mesh | Eosinophils | - |
dc.subject.mesh | Leukotriene Antagonists - administration & dosage - pharmacokinetics | - |
dc.title | Anti-inflammatory effects of high-dose montelukast in an animal model of acute asthma | - |
dc.type | Article | - |
dc.identifier.email | Wu, AY: adrianwu@hku.hk | - |
dc.identifier.email | Chik, SC: chikscc@hkucc.hku.hk | - |
dc.identifier.email | Li, Z: zzli@hkuspace.hku.hk | - |
dc.identifier.email | Tsang, KW: kwttsang@hkucc.hku.hk | - |
dc.identifier.doi | 10.1046/j.1365-2222.2003.01615.x | - |
dc.identifier.pmid | 12614451 | - |
dc.identifier.scopus | eid_2-s2.0-0037338372 | - |
dc.identifier.hkuros | 100315 | - |
dc.identifier.volume | 33 | - |
dc.identifier.issue | 3 | - |
dc.identifier.spage | 359 | - |
dc.identifier.epage | 366 | - |
dc.identifier.isi | WOS:000181330600016 | - |
dc.publisher.place | United Kingdom | - |
dc.identifier.issnl | 0954-7894 | - |