National Academy of Sciences, Proceedings of the National Academy of Sciences, 10(114), 2017
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Significance Inhaled particulates, such as multiwalled carbon nanotubes, can induce neuroinflammatory outcomes. The present study shows that acute neuroinflammation is dependent on the impairment of blood-brain barrier function. Pharmacologic restoration of blood-brain barrier integrity prevented the neuroinflammatory responses to pulmonary multiwalled carbon nanotube exposure. Circulating factors, including possibly thrombospondin-1, recapitulate inflammatory responses in cultured cerebrovascular endothelial cells, suggesting a mechanism for indirect systemic effects of inhaled nanoparticles.