Study on the relationship between PM2.5 with lung inflammation and asthma
學生姓名:
曾宇婷
指導教授:
吳彰哲
學期:
107上
摘 要:
Asthma is a chronic inflammatory and allergic disease. At present, asthma has been confirmed to be closely related to Th2 (Helper T cell type 2) cytokines. Th2 cytokines, including IL-4 (Interleukin 4), IL-5, and IL-13, induce B cells to produce specific IgE and cause allergy. There are many factors in the environment that can cause asthma, like PM2.5 (Particular matter 2.5) is also one of the asthma allergens. PM2.5 means particle diameter is ≤ 2.5 μm, it has been confirmed that it can cause inflammation or lung cancer caused by inflammation in the lungs of the human body, and finally cause pulmonary fibrosis. Also, PM2.5 can lead to oxidative stress, finally made cell damage. This report explores the association of PM 2.5 with inflammation and asthma. PM2.5 can adsorb various organic substances, including PAHs (Polycyclic hydrocarbons), transition metals, endotoxin. PM2.5 in BEAS-2B cells could cause DNA broken, by producing ROS (Reactive oxygen species), MMP (Mitochondrial membrane potential) would decrease resulting in cell apoptosis. Add PM2.5 in BALB/C male mice, which was induced asthma by OVA (ovalbumin). The levels of inflammation factors (Interleukin-1 β, IL-1β、Tumor necrosis factor alpha, TNF-α), TH2 related cytokines (IL-5), factors (IL-6, IL-17A, IL-25) and IgE would increase in lung. The enzyme of HO-1 (Heme oxygenase-1) is related to oxidative stress. The greater the oxidative pressure, the higher HO27 1 expression. The results show of that HO-1 expression was also raised. These findings suggested that PM2.5 would make the inflammation worse and might play an adjuvant in animal experiment. By extending allergens affecting time as well as enhanced the levels of inflammation factors and Th2 cells cytokines.
專題討論20181017_曾宇婷-摘要.pdf