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Etsushi Kuroda
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Hyogo Medical University

Bio: I completed my studies at Kyushu Institute of Technology and Hiroshima University Graduate School, and obtained a PhD from the University of Occupational and Environmental Health, Japan (UOEH). I gained experience as an assistant professor and lecturer in UOEH, and then conducted research abroad at the Terry Fox laboratory in the British Columbia Cancer Research Centre, Canada. In 2012, I was appointed as a Specially Appointed Associate Professor at the Immunology Frontier Research Center (IFReC) of Osaka University. From 2017, I served as a Senior Researcher and Project Leader at the National Institutes of Biomedical Innovation, Health and Nutrition (NIBIOHN). Since 2019, I have held my current position as Professor and Chair at Hyogo Medical University School of Medicine.

 

Abstract: Inhaled fine particles, such as PM2.5 and sand dusts, activate immune responses in the airway and contribute to inflammatory diseases. While some inorganic fine particles stimulate immune responses, the underlying mechanisms of immune modulation by these particles remain unclear. Fine particles reach deep into the lungs by inhalation. It is generally believed that they are engulfed by alveolar macrophages to facilitate clearance. In this study, we investigated the effects of fine particles on alveolar macrophages using two distinct types of fine particles: inflammatory particles, which induce allergic inflammation in the lungs, and non-inflammatory particles, which do not induce inflammation after the inhalation. Our findings revealed that inflammatory particles stimulate alveolar macrophages to induce interleukin-1alpha (IL-1a). IL-1a was released by macrophage cell death and plays a key role in allergic inflammation. In contrast, non-inflammatory particles do not induce cell death or the release of inflammatory molecules. These results suggest that alveolar macrophage death caused by inhaled fine particles is closely linked to particle-induced allergic inflammation through damage-associated molecular patterns (DAMPs) release from dying cells. In this talk, I will present the detailed mechanisms of DAMPs release from alveolar macrophages as well as the physicochemical difference between inflammatory and non-inflammatory particles.


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Date Time Local Time Room Forum Session Role Topic
2025-10-17 11:30-11:50 2025-10-17,11:30-11:50Room 5 - Guibin Hall 1 Symposium Program (Session)

Session 23: Mechanisms of Immune System Toxicity and Therapeutic Approaches for Modifying Disease

Speaker Molecular machinery of particle-caused inflammation and allergy in lung immunity