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Atypical Microglial Response to Biodiesel Exhaust in Healthy and Hypertensive Rats
Citation:
Mumaw, C., M. Surace, S. Levesque, U. Kodavanti, P. Kodavanti, J. Royland, AND M. Block. Atypical Microglial Response to Biodiesel Exhaust in Healthy and Hypertensive Rats. NEUROTOXICOLOGY. Elsevier B.V., Amsterdam, Netherlands, 59:155-163, (2017).
Impact/Purpose:
Biodiesel exhaust health effects are important as it is widely used as a renewable energy source. Evidence points to a link between high levels of urban air pollution and several central nervous systems(CNS) conditions such as stroke, Alzheimer's disease and decreased cognitive function. The study here demonstrates that biodiesel can affect microglia, which are the resident innate immune cells in the brain, essential for healthy CNS function. At present, it is unclear whether this microglial/CNS response is benign, beneficial, or deleterious. The underlying mechanisms and the consequences of this unusual response remains of significant scientific interest in the ongoing effort to understand the potential impact of urban air pollution on CNS health.
Description:
Accumulating evidence suggests a deleterious role for urban air pollution in central nervous system (CNS) diseases and neurodevelopmental disorders. Microglia, the resident innate immune cells and sentinels in the brain, are a common source of neuroinflammation and are implicated air pollution-induced CNS effects. While renewable energy, such as soy-based biofuel, is of increasing public interest, there is little information on how soy biofuel may affect the brain. especially in people with preexisting conditions. To address this, male spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto (WKY) rats were exposed to 100% Soy Biodiesel Exhaust (100SBE; 0, 50, 150 and 500 μg/m3) by inhalation for 4 h/day for 4 weeks (5 days/week). Ionized calcium-binding adapter molecule- 1(IBA-1) staining of microglia in the substantia nigra revealed significant changes in morphology with 100SBE exposure in rats from both genotypes where SHR were less sensitive. Aconitase activity was inhibited in the frontal cortex and cerebellum of WKY rats exposed to 100SBDE. No consistent changes occurred in pro-inflammatory cytokine expression, nitrated protein, or arginase1 expression in brain regions from either rat strain exposed to 100SBE. However, while IBA-1 mRNA expression was not modified, CX3CR1 mRNA expression was lower in the striatum of 100SBE exposed rats regardless of genotype, suggesting a downregulation of the fractalkine receptor on microglia in this brain region. Together, these data indicate that while microglia are detecting and responding to 100SBDE exposure with changes in morphology there is reduced expression of CX3CR1 regardless of genetic background and the activation response is atypical without traditional inflammatory markers of M1 or M2 activation in the brain.
