title: Immunomodulatory effects of oak dust exposure in a murine model of allergic asthma.
abstract: Repeated airway exposure to wood dust has been reported to cause adverse respiratory effects such as asthma and chronic bronchitis. In our recent study, we found that exposure of mice to oak dust induced more vigorous lung inflammation compared to birch dust exposure. In the present study, we assessed the immunomodulatory effects of repeated intranasal exposure to oak dust both in nonallergic and in ovalbumin-sensitized, allergic mice. Allergen-induced influx of eosinophils and lymphocytes was seen in the lungs of allergic mice. Oak dust exposure elicited infiltration of neutrophils, lymphocytes, and macrophages in nonallergic mice. Interestingly, oak dust-induced lung neutrophilia as well as oak dust-induced production of the proinflammatory cytokine TNF-alpha and chemokine CCL3 were significantly suppressed in allergic mice. On the other hand, allergen-induced expression of IL-13 mRNA and protein was significantly reduced in oak dust-exposed allergic mice. Finally, allergen-induced airway hyperreactivity to inhaled metacholine was significantly suppressed in oak dust-exposed allergic mice. The present results suggest that repeated airway exposure to oak dust can regulate pulmonary inflammation and airway responses depending on the immunological status of the animal.
authors.affiliation: Unit of Excellence in Immunotoxicology, Team for Biological Mechanisms and Prevention of Work-related Diseases, Finnish Institute of Occupational Health, Helsinki, Finland.
authors.forename: Juha
authors.initials: J
authors.lastname: Määttä
authors.forename: Rita
authors.initials: R
authors.lastname: Haapakoski
authors.forename: Maili
authors.initials: M
authors.lastname: Lehto
authors.forename: Marina
authors.initials: M
authors.lastname: Leino
authors.forename: Sari
authors.initials: S
authors.lastname: Tillander
authors.forename: Kirsti
authors.initials: K
authors.lastname: Husgafvel-Pursiainen
authors.forename: Henrik
authors.initials: H
authors.lastname: Wolff
authors.forename: Kai
authors.initials: K
authors.lastname: Savolainen
authors.forename: Harri
authors.initials: H
authors.lastname: Alenius
mesh_terms: D000818:Animals; D001249:Asthma / Q000139:chemically induced / Q000276:immunology* / Q000378:metabolism; D016535:Bronchial Hyperreactivity / Q000139:chemically induced / Q000276:immunology* / Q000378:metabolism; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D019742:Chemokines, CC / Q000235:genetics / Q000378:metabolism; D004195:Disease Models, Animal; D004391:Dust; D005260:Female; D019570:Inhalation Exposure / Q000009:adverse effects*; D018793:Interleukin-13 / Q000235:genetics / Q000378:metabolism; D007962:Leukocytes / Q000187:drug effects / Q000276:immunology; D008168:Lung / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D019402:Macrophage Inflammatory Proteins / Q000235:genetics / Q000378:metabolism; D008264:Macrophages / Q000187:drug effects / Q000276:immunology; D016210:Methacholine Chloride; D051379:Mice; D008807:Mice, Inbred BALB C; D020556:Neutrophil Infiltration / Q000187:drug effects / Q000276:immunology; D010047:Ovalbumin / Q000276:immunology / Q000633:toxicity; D029963:Quercus; D012333:RNA, Messenger / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014934:Wood
chemical_list: C496534:Ccl3 protein, mouse; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D019742:Chemokines, CC; D004391:Dust; D018793:Interleukin-13; D019402:Macrophage Inflammatory Proteins; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D016210:Methacholine Chloride; D010047:Ovalbumin