title: Effects of Ecklonia cava ethanolic extracts on airway hyperresponsiveness and inflammation in a murine asthma model: role of suppressor of cytokine signaling.
abstract: Ecklonia cava (EC) is a brown alga that evidences radical scavenging activity, bactericidal activity, tyrosinase inhibitory activity, and protease inhibitory activity. However, its anti-allergic effects remain poorly understood. In the current study, we attempted to determine whether pretreatment with EC induces a significant inhibition of asthmatic reactions in a mouse asthma model. Mice sensitized and challenged with ovalbumin (OVA) evidenced typical asthmatic reactions, as follows: an increase in the number of eosinophils in bronchoalveolar lavage fluid; a marked influx of inflammatory cells into the lung around blood vessels and airways, and airway luminal narrowing; the development of airway hyperresponsiveness; the detection of tumor necrosis factor-alpha (TNF-alpha) and Th2 cytokines, including IL-4 and IL-5 in the bronchoalveolar lavage (BAL) fluid; and the detection of allergen-specific immunoglobulin E (IgE) in the serum. However, the administration of EC extract prior to the final airway OVA challenge resulted in a significant inhibition of all asthmatic reactions. We also demonstrated that EC extracts treatment resulted in significant reductions on matrix metalloproteinase-9 (MMP-9) and Suppressor of cytokine signaling-3 (SOCS-3) expression and a reduction in the increased eosinophil peroxidase (EPO) activity. The treatment of animals with EC extracts resulted in a significant reduction in the concentrations of the Th2 cytokine (IL-4 and IL-5) in the airways, without any concomitant increase in the concentration of Th1 cytokines. These findings indicate that EC extracts may prove useful as an adjuvant therapy for allergic airway reactions via the inhibition of the Th2 response. Accordingly, this study may provide evidence that EC extract performs a critical function in the amelioration of the pathogenetic process of asthma in mice.
authors.affiliation: Marine Bioprocess Research Center, Pukyong National University, Busan 608-737, Republic of Korea.
authors.forename: Se-Kwon
authors.initials: SK
authors.lastname: Kim
authors.forename: Da-Young
authors.initials: DY
authors.lastname: Lee
authors.forename: Won-Kyo
authors.initials: WK
authors.lastname: Jung
authors.forename: Ji-Hye
authors.initials: JH
authors.lastname: Kim
authors.forename: Inhak
authors.initials: I
authors.lastname: Choi
authors.forename: Sae-Gwang
authors.initials: SG
authors.lastname: Park
authors.forename: Su-Kil
authors.initials: SK
authors.lastname: Seo
authors.forename: Soo-Woong
authors.initials: SW
authors.lastname: Lee
authors.forename: Chang Min
authors.initials: CM
authors.lastname: Lee
authors.forename: Sung Su
authors.initials: SS
authors.lastname: Yea
authors.forename: Yung Hyun
authors.initials: YH
authors.lastname: Choi
authors.forename: Il-Whan
authors.initials: IW
authors.lastname: Choi
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000276:immunology / Q000627:therapeutic use*; D001249:Asthma / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism; D016535:Bronchial Hyperreactivity / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000276:immunology; D016085:Bronchoconstrictor Agents / Q000494:pharmacology; D016207:Cytokines / Q000378:metabolism*; D047209:Eosinophil Peroxidase / Q000378:metabolism; D000431:Ethanol; D005260:Female; D007073:Immunoglobulin E / Q000097:blood; D019278:Matrix Metalloproteinase 3 / Q000096:biosynthesis; D016210:Methacholine Chloride / Q000494:pharmacology; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin; D000459:Phaeophyceae / Q000737:chemistry*; D008517:Phytotherapy; D010936:Plant Extracts / Q000627:therapeutic use; D012997:Solvents; D000071223:Suppressor of Cytokine Signaling 3 Protein; D050826:Suppressor of Cytokine Signaling Proteins / Q000096:biosynthesis