The role of pro-/anti-inflammation imbalance in Aβ42 accumulation of rat brain co-exposed to fine particle matter and sulfur dioxide

Abstract

Taiyuan is a center of coal-based electricity production and many chemicals industries, where mixtures of sulfur dioxide (SO₂) and particulate matter may be more prominent. The focus of the present study was to determine if there is a link between adverse effects in the brain and the combined-exposure to SO₂ and fine particulate matter (PM_2.5). Rats were exposed alternately to PM_2.5 with different dosages (1.5, 6.0 and 24.0 mg/kg body weight) and SO₂ at the level of 5.6 mg/m³. The results showed that the combined exposure to PM_2.5 and SO₂ enhanced the mRNA expression and protein level of TNF-α and IL-6 in rat cortex and hippocampus relative to the control, SO₂ and PM_2.5 alone. Instead, TGF-β1 mRNA and protein level were down-regulated in the brain. Additionally, PM_2.5 at medium and/or high dose caused marked increase in Aβ42 level and PM_2.5 + SO₂ induced further increase of Aβ42 level in the cortex and hippocampus. It suggests that SO₂ and PM_2.5 can synergistically exert inflammation responses and induce Aβ42 accumulation in the brain. Also, it is notable that the Aβ42 accumulation of rat cortex and hippocampus were closely associated with pro-/anti-inflammatory cytokines ratio. These results clearly demonstrated that the combined exposure to PM_2.5 and SO₂ can induce the imbalance of pro-/anti-inflammatory cytokine, resulting in Aβ42 accumulation of rat brain cortex and hippocampus.

Keywords:

• Fine particulate matter
• sulfur dioxide
• inflammatory response
• Aβ42 deposition

Disclosure statement

The authors report no conflict of interest. The authors alone are responsible for the content and writing of the paper.

Additional information

Funding

This research was supported by grants from the National Natural Science Foundation of China (21405099, 11274340, 91543202) and Nature Science Foundation of Shanxi Province in China (2014011036-2, 201601D202087).