title: Crude extracts of Caenorhabditis elegans suppress airway inflammation in a murine model of allergic asthma.
abstract: Epidemiological studies suggest an inverse relationship between helminth infections and allergic disease, and several helminth-derived products have been shown to suppress allergic responses in animals. This study was undertaken to evaluate the effect of a crude extract of Caenorhabditis elegans on allergic airway inflammation in a murine model of asthma. Allergic airway inflammation was induced in BALB/c mice by sensitization with ovalbumin. The effect of the C. elegans crude extract on the development of asthma and on established asthma was evaluated by analyzing airway hyperresponsiveness, serum antibody titers, lung histology and cell counts and cytokine levels in the bronchoalveolar lavage fluid. The role of IFN-γ in the suppression of asthma by the C. elegans crude extract was investigated in IFN-γ knockout and wild-type mice. When mice were sensitized with ovalbumin together with the crude extract of C. elegans, cellular infiltration into the lung was dramatically reduced in comparison with the ovalbumin-treated group. Treatment of mice with the C. elegans crude extract significantly decreased methacholine-induced airway hyperresponsiveness and the total cell counts and levels of IL-4, IL-5 and IL-13 in the bronchoalveolar lavage fluid but increased the levels of IFN-γ and IL-12. Sensitization with the C. elegans crude extract significantly diminished the IgE and IgG1 responses but provoked elevated IgG2a levels. However, the suppressive effect of the C. elegans crude extract was abolished in IFN-γ knockout mice, and the Th2 responses in these mice were as strong as those in wild-type mice sensitized with ovalbumin. The crude extract of C. elegans also suppressed the airway inflammation associated with established asthma. This study provides new insights into immune modulation by the C. elegans crude extract, which suppressed airway inflammation in mice not only during the development of asthma but also after its establishment by skewing allergen-induced Th2 responses to Th1 responses.
authors.affiliation: Department of Parasitology and Tropical Medicine, Seoul National University College of Medicine, and Institute of Endemic Diseases, Seoul National University Medical Research Center, Seoul, Korea.
authors.forename: Sung Eun
authors.initials: SE
authors.lastname: Kim
authors.forename: Jae-Hwan
authors.initials: JH
authors.lastname: Kim
authors.forename: Byung-Hoon
authors.initials: BH
authors.lastname: Min
authors.forename: Young Mee
authors.initials: YM
authors.lastname: Bae
authors.forename: Sung-Tae
authors.initials: ST
authors.lastname: Hong
authors.forename: Min-Ho
authors.initials: MH
authors.lastname: Choi
mesh_terms: D000818:Animals; D000906:Antibodies / Q000097:blood; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D017173:Caenorhabditis elegans / Q000737:chemistry*; D002452:Cell Count; D045424:Complex Mixtures / Q000032:analysis / Q000494:pharmacology* / Q000627:therapeutic use; D016207:Cytokines / Q000276:immunology; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D007371:Interferon-gamma / Q000235:genetics / Q000276:immunology; D008168:Lung / Q000473:pathology; D016210:Methacholine Chloride; D051379:Mice; D008807:Mice, Inbred BALB C; D018345:Mice, Knockout; D010047:Ovalbumin; D012130:Respiratory Hypersensitivity / Q000188:drug therapy* / Q000276:immunology
chemical_list: D000906:Antibodies; D045424:Complex Mixtures; D016207:Cytokines; D016210:Methacholine Chloride; D007371:Interferon-gamma; D010047:Ovalbumin