Polycyclic aromatic hydrocarbons in urban particle matter exacerbate movement disorder after ischemic stroke via potentiation of neuroinflammation

Abstract

Background A recent epidemiological study showed that air pollution is closely involved in the prognosis of ischemic stroke. We and others have reported that microglial activation in ischemic stroke plays an important role in neuronal damage. In this study, we investigated the effects of urban aerosol exposure on neuroinflammation and the prognosis of ischemic stroke using a mouse photothrombotic model. Results When mice were intranasally exposed to CRM28, urban aerosols collected in Beijing, China, for 7 days, microglial activation was observed in the olfactory bulb and cerebral cortex. Mice exposed to CRM28 showed increased microglial activity and exacerbation of movement disorder after ischemic stroke induction. Administration of core particles stripped of attached chemicals from CRM28 by washing showed less microglial activation and suppression of movement disorder compared with CRM28-treated groups. CRM28 exposure did not affect the prognosis of ischemic stroke in null mice for aryl hydrocarbon receptor, a polycyclic aromatic hydrocarbon (PAH) receptor. Exposure to PM2.5 collected at Yokohama, Japan also exacerbated movement disorder after ischemic stroke. Conclusion Particle matter in the air is involved in neuroinflammation and aggravation of the prognosis of ischemic stroke; furthermore, PAHs in the particle matter could be responsible for the prognosis exacerbation.

Decreases in the number of microglia and neural circuit dysfunction elicited by developmental exposure to neonicotinoid pesticides in mice

“…The brain was isolated and cryoprotected in 30% sucrose, and then was frozen in powdered dry ice, and 50‐μm‐thick floating sections including hippocampus area were prepared using a Cryostat (CM3050 S; Leica Biosystems). The brain sections were stained with Iba1, CD68, and DAPI to calculate the number of microglia, the microglial soma area and CD68 expression in microglia, according to our previous reports 19,20 . The antibodies used in this study were listed in Table 1.…”

“…The brain sections were stained with Iba1, CD68, and DAPI to calculate the number of microglia, the microglial soma area and CD68 expression in microglia, according to our previous reports. 19,20 The antibodies used in this study were listed in Table 1. Stained sections were observed laser-scanning microscopy (LSM700; Carl Zeiss, Oberkochen, Germany).…”

A simple air–liquid interface exposure system for exposing cultured human 3D epidermis and cornea to PM2.5 collected through cyclonic separation

“…Metal contents in PM2.5 were measured by IDEA Consultants, Inc. (Tokyo, Japan) using inductively coupled plasma-mass spectrometry. PAHs in PM2.5 were determined using GC-MS (7890A/5957C, Agilent, Palo Alto, CA, USA) according to our previous report (Tanaka et al, 2023). Endotoxin levels in the PM2.5 were measured using an Endospecy ES-50M set (Seikagaku Co., Tokyo, Japan) according to the manufacturer's protocol.…”

Exposure to Environmental Toxins: Potential Implications for Stroke Risk via the Gut– and Lung–Brain Axis

“…Exposure to BaP has a direct effect on brain function since BaP and its metabolites can accumulate in lipid-rich tissues such as the brain [68] and have been shown to impair the blood-brain barrier function [69]. Tanaka et al demonstrated that exposure to PAHs altered stroke outcomes in mice after intranasal exposure, which induced edema in the brain and impaired locomotor functions in rats [70]. These findings suggest that despite the liver's primary role in detoxifying xenobiotics [71], there exists a tissue-specific vascular response, potentially highlighting the link between certain PAHs and stroke pathophysiology.…”

“…Further evidence supports the idea that environmental toxins can alter the lung-brain axis and may influence the likelihood of stroke onset and post-stroke outcomes. Tanaka et al demonstrated that intranasal exposure to urban aerosols in mice can affect post-stroke recovery by augmenting neuroinflammation, activating brain resident microglial cells, and impairing motor function post-stroke [70].…”