Immunomodulatory Effects of Oak Dust Exposure in a Murine Model of Allergic Asthma

Repeated airway exposure to wood dust has been reported to causeadverse respiratory effects such as asthma and chronic bronchitis.In our recent study, we found that exposure of mice to oak dustinduced more vigorous lung inflammation compared to birch dustexposure. In the present study, we assessed the immunomodulatoryeffects of repeated intranasal exposure to oak dust both innonallergic and in ovalbumin-sensitized, allergic mice. Allergen-inducedinflux of eosinophils and lymphocytes was seen in the lungsof allergic mice. Oak dust exposure elicited infiltration ofneutrophils, lymphocytes, and macrophages in nonallergic mice.Interestingly, oak dust–induced lung neutrophilia as wellas oak dust–induced production of the proinflammatorycytokine TNF- and chemokine CCL3 were significantly suppressedin allergic mice. On the other hand, allergen-induced expressionof IL-13 mRNA and protein was significantly reduced in oak dust–exposedallergic mice. Finally, allergen-induced airway hyperreactivityto inhaled metacholine was significantly suppressed in oak dust–exposedallergic mice. The present results suggest that repeated airwayexposure to oak dust can regulate pulmonary inflammation andairway responses depending on the immunological status of theanimal.