Particles such as an asian sand dust activate autophagic and apoptotic key molecules in CD11b positive cells. (106.6)

Abstract

Abstract Asian sand dust (ASD) is derived from air pollutants in East China and has a long history of appearing in Japan. Recently, it is knowing that ASD contains microbial materials, sulfate (SO(4)(2-)) and nitrate (NO(3)(-)), therefore there is increasing concern for its possible adverse health effects. Although it has been reported that ASD induces inflammatory responses in the lung tissue and causes respiratory diseases such as eosinophilia in mice, the effect of ASD on the peripheral lymphoid organ are not fully understood. In this study, we examine the effect of ASD on immune system. ICR mice were administered intratracheal ASD (0, 0.2, 0.02 mg/mice), and were sacrificed at 4 weeks (1 time per week and total 4 times) after administration. Spleen cells were prepared and cell lysates of splenocytes were resolved in western blotting. Immuno-blotting demonstrated that ASD induced autophagic-maker LC3 and p62 expression and also induced PARP cleavage suggesting caspase-dependent apoptosis in splenocytes. In addition, ASD could increase the expression of TNF-α mRNA analyzed by Real-time PCR. As same as in vivo, we observed ASD enhanced TNF-α production induced by ConA in splenocytes. Taken together, ASD induced systemic inflammation resulting in autophagic and apoptotic phenomena in splenocytes, suggesting that ASD administration not only triggered pulmonary inflammation but also affected peripheral lymphoid tissue.