Title:
Molecular mechanisms of particulate-induced pulmonary inflammation
～Intrinsic adjuvant and allergy～

Etsushi Kuroda
Laboratory of Vaccine Science, WPI Immunology Frontier Research Center, Osaka University

Abstract:
Recently, the number of patients suffering from allergic diseases such as asthma or rhinitis has increased especially in developed country. The reason is unclear, but a lot of papers have shown that particle pollutant such as diesel exhaust and sand dust may be involved in the exacerbation of allergic responses. Furthermore, it is thought that several nanometer- to micrometer-sized tiny particulates, such as particulate matter 2.5 (PM2.5) that is less than 2.5 micrometers in diameter, could enter into the respiratory tract and settle deep in lungs, causing pulmonary chronic inflammation in lung such as asthma. Some particulates and crystals are known to stimulate immune systems to induce type 2 inflammatory responses, which are characterized by the accumulation of eosinophils and the elevation of antigen-specific serum IgE amounts in vivo. Most particulates including particle pollutant are considered to work as immune adjuvants and enhance allergen-specific type 2 responses. However, the basis for the adjuvanticity of these particulates and the mechanisms by which they elicit type 2 responses remain poorly understood.
 Recently, we established a particulate-induced lung inflammation model by intratracheal instillation of particulates, and found that damage-associated molecular patterns (DAMPs) triggered lung inflammation and IgE induction. In this seminar, we will show the underlying mechanisms of particulate-induced type 2 responses, from the point of view of DAMPs (intrinsic adjuvant).