It is known that inhaled fine particles such as particle pollutions are associated with allergic responses. Many reports have shown that some particulates function as adjuvant to enhance immune responses, however its underlying mechanisms are still unclear. Here, we will show how particulates induce immune responses in the lungs.
We used aluminium salt (alum) and crystalline silica as inflammatory particulate. These inflammatory particulates stimulated alveolar macrophage to release interleukin-1α (IL-1α) through cell death. We also observed IL-1α release in the bronchoalveolar lavage fluid (BALF) after intratracheal instillation (i.t.) of inflammatory particulate alum in vivo. Released IL-1α in the lungs was thought to be a damage-associated molecular pattern (DAMP) and contributed to antigen-specific IgE production in mouse model of particulate-induced allergic inflammation. In addition, we found the lymphoid cluster formations in the lungs after i.t. alum instillation and allergen exposure. This lymphoid cluster was considered to be inducible bronchus-associated lymphoid tissue (iBALT), and we suggest that iBALT formation might be an important role for local IgE responses in the lungs.
These results indicate that inhalation of particulates and allergen exposure induces and exacerbate allergic responses though the unique immune responses in the lungs such as alveolar macrophage death and iBALT formation.