Identification of the mechanisms driving the onset of chronic inflammation by cigarette smoke

2016 Fiscal Year Final Research Report

• Project/Area Number: 25430182
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: System genome science
• Research Institution: Osaka University
• Principal Investigator: Diez Diego 大阪大学, 免疫学フロンティア研究センター, 准教授 (90597741)
• Project Period (FY): 2013-04-01 – 2017-03-31
• Keywords: Systems biology / Immunology / Bioinformatics

Outline of Final Research Achievements

Exposure to tobacco and silica leads to Chronic Obstructive Pulmonary Disease and silicosis respectively, diseases marked by chronic inflammation and progression. This project aims to understand the mechanisms leading to chronic inflammation in a silicosis model. We expose mice to different silica doses for one month, then monitor disease progression in the lungs over one year. We measure immune cells number and gene expression 1, 3 and 12 months after exposure. Mice exposed to high silica doses during the first month show higher levels of inflammatory chemokines and recruitment of T cells after one year. Transcriptomic analysis identified 82 genes differentially expressed, with a prominent role of the antigen processing and presentation pathway.

Free Research Field

総合生物