AAAR 36th Annual Conference October 16 - October 20, 2017 Raleigh Convention Center Raleigh, North Carolina, USA
Abstract View
Pro-inflammatory Effects of PM2.5 from Beijing Winter Haze: Revealing the Role of Individual External and Internal Microbiome
SHEN FANGXIA, Liu Fobang, Zhang Xiangyu, Li Jing, Ziegler Kira, Ting Zhang, Zhu Tianle, Manabu Shiraiwa, Maosheng Yao, Haijie Tong, Kurt Lucas, Ulrich Pöschl, Beihang University
Abstract Number: 728 Working Group: Linking Aerosol Oxidative Potential with Chemical Composition and Biological Endpoints
Abstract China has experienced frequent serious haze episodes in recent years, which accordingly has led to increasing number of studies regarding its formation mechanisms. On the other hand, the public is becoming more concerned about the health impact of the haze problems. Oxidative stress and inflammation is generally accepted mechanism by which air pollutants cause adverse health effects. However, the molecular level mechanism is far away from clear. Human microbiome, which composes 10 times more microorganisms than our own cells, has gained increasing attention in its roles in people’s health. In particular, components from our resident microbiome, i.e., lipopolysaccharide (LPS), play an important role in regulating immune homeostasis. This study aims to investigate the potential synergistic role of air pollutants and microbial components, and relevant results could further shed new light on the understanding of the mechanism.
Particulate matters smaller than 2.5 μm (PM2.5) collected in Beijing during 2016 winter haze period were used to stimulate THP-1-derived macrophages. The cellular immune response was evaluated by measuring the cytokine production, including IL-1b, IL-8, TNF and IL-6. To simulate the internal body microenvironment exposure, elevated LPS of different concentrations together with PM2.5 water extractions was applied to study the cellular response. No toxicity was detected when 10 μg/ml PM2.5 water extractions were given to the macrophages. The pro-inflammatory immune effect of PM2.5 collected on days of different pollution levels varies, however, it was not induced by the cytotoxicity. Characterization results of PM2.5 indicated that this discrepancy in cellular inflammatory response was attributed to particle-borne LPS and metal levels (Fe and Ni). Furthermore, the pro-inflammatory cytokine secretion was augmented when macrophages were stimulated with PM2.5 in the presence of elevated lipopolysaccharide (LPS). Samples collected from heavily polluted episodes show stronger enhancing pro-inflammatory effects when 100 pg/ml LPS was applied. Whereas, the enhancing effect was weak in the presence of either 1 or 10 pg/ml LPS. PCR array assay results suggest that oxidative stress plays vital role in the magnifying effects of PM2.5. Knowing the body internal microenvironment can be of great importance to evaluating the PM2.5 health effects. The results obtained here provide an evidence about the synergistic effects of PM2.5 and microbial LPS. Overall, this study highlights the importance of studying roles of human microbial structures, especially respiratory microbiome, when unraveling the underlying mechanism at cellular and molecular level.