Atmospheric fine particles (PM2.5, yellow sand, diesel particles, etc.) are one of the various factors involved in allergic diseases.Many research reports have revealed that fine particles in the atmosphere have an "anti-adjuvant effect" (an action that enhances the immune response to allergens [antigen substances that cause allergies]) that induces and exacerbates allergic inflammation. However, the detailed mechanism was unknown.

　When inhaled fine particles such as PM2.5, they reach the depths of the respiratory tract and cause an inflammatory reaction, and in response, alveolar macrophages in the lungs phagocytose the fine particles and expel them out of the body.Therefore, this time, we used alveolar macrophages collected from mice to phagocytose various fine particles.As a result, alveolar macrophages caused cell death only when they phagocytosed the fine particles (aluminum salt and silica) that caused allergic inflammation, and released an immunostimulatory substance called IL-1alpha.When fine particles are administered to the lungs of mice, IL-1alpha continues to be released into the lungs for two weeks, during which inhalation of allergens induces IgE (immunoglobulin E), which is one of the causative factors of allergies. Was done.This indicates that when fine particles are inhaled, they remain susceptible to allergens for a long period of time.In addition, lymphoid tissue called ectopic lymph nodes was formed in the lungs, suggesting that it may be involved in IgE induction.

　With this achievement, it is expected to develop a new treatment method for allergic inflammation caused by PM2.5 and yellow sand by controlling the immunostimulatory factors induced by fine particles.