Effects of non-protein-type amino acids of fine particulate matter on E-cadherin and inflammatory responses in mice

• PM2.5 was collected from Beijing, Xian and Hong Kong during haze episodes.
• OC, EC and free amino acids of PM2.5 were characterised.
• BALB/c mice were received an aspiration exposure of PM2.5.
• PM2.5 caused pulmonary inflammation and E-cadherin inhibition.
• Non-protein type amino acids were associated with inflammation.

Exposure to particulate matter less than 2.5 μm (PM2.5) in size is an urgent issue for the protection of human health. Chemicals with PM2.5 collected during a period of intensive haze episodes in Beijing (BJ), Xian (XA) and Hong Kong (HK) were characterised for organic carbon (OC), elemental carbon (EC), total carbon (TC) and free amino acids. BALB/c mice underwent aspiration exposure of 50 or 150 μg of PM2.5/mouse (BJ, XA and HK) on days 1 and 7 and were euthanised on day 14. The effects of these exposures on E-cadherin and inflammatory responses in the mouse lungs were analysed. The PM2.5 chemicals consisted of significant amounts of OC: 36.6 ± 17.2 μg/m3 for BJ, 38.8 ± 3.8 μg/m3 for XA and 7.2 ± 1.4 μg/m3 for HK. A total of 23 free amino compounds for the PM2.5 samples were analysed: 4075 ± 1578 pmol/m3 for BJ, 4718 ± 2190 pmol/m3 for XA and 1145 ± 213 pmol/m3 for HK. Exposure to PM2.5 resulted in the suppression of E-cadherin levels in the lung tissues and increased IFN-γ, IL-2, IL-4, IL-6 and IL-10 in the bronchoalveolar lavage fluid. The alterations in E-cadherin, IFN-γ, IL-6 and IL-10 were associated with OC, TC and some amino acids, particularly non-protein-type amino acids. These data emphasised the deleterious health effects of PM2.5.