Epidemiologic studies suggest a causal relationship between the increase in allergic airway disease and air pollution. The aim of this study was to investigate mechanisms through which particles modulate pulmonary immune responses against antigens.

Mice were exposed intranasally to ovalbumin (OVA) and Carbon Black (CB), as a model particle for particulate air pollution, for 3 consecutive days. Lymphocytes were isolated from the lungs and the airway draining lymph nodes and the spleen 4 days after the last exposure, and cultured for 96 hours with media or media containing 100ug OVA/ml. Cytokines were analyzed in culture supernatants. The lung and draining lymph nodes were also studied morphologically.

Co-exposure to CB and OVA results in antigen-specific cytokine production by lymphocytes from the lungs, lung draining lymph nodes and spleen but not the nose draining lymph nodes. The cytokine profile shows a clear Th2 response with high levels of IL-5 and IL-4 and relatively low IFN-gamma levels. Lungs and lung draining lymph nodes show CB containing macrophages.

These data indicate that administration of particulate matter via the airways adjuvates for a systemic Th2 immune response to a bystander antigen. Further mechanistic studies will be performed to study the role of the CB containing macrophages isolated from the lungs and the draining lymph nodes.