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Hypoxia augments LPS-induced inflammation and triggers high altitude cerebral edema in mice

Chen

Hypoxia augments LPS-induced inflammation and triggers high altitude cerebral edema in mice Thumbnail


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Abstract

Abstract High altitude cerebral edema (HACE) is a life-threatening illness that develops during the rapid ascent to high altitudes, but its underlying mechanisms remain unclear. Growing evidence has implicated inflammation in the susceptibility to and development of brain edema. In the present study, we investigated the inflammatory response and its roles in HACE in mice following high altitude hypoxic injury. We report that acute hypobaric hypoxia induced a slight inflammatory response or brain edema within 24 h in mice. However, the lipopolysaccharide (LPS)-induced systemic inflammatory response rapidly aggravated brain edema upon acute hypobaric hypoxia exposure by disrupting blood-brain barrier integrity and activating microglia, increasing water permeability via the accumulation of aquaporin-4 (AQP4), and eventually leading to impaired cognitive and motor function. These findings demonstrate that hypoxia augments LPS-induced inflammation and induces the occurrence and development of cerebral edema in mice at high altitude. Here, we provide new information on the impact of systemic inflammation on the susceptibility to and outcomes of HACE.

Acceptance Date Apr 17, 2017
Publication Date Apr 20, 2017
Journal Brain, Behavior, and Immunity
Print ISSN 0889-1591
Publisher Elsevier
Pages 226-275
DOI https://doi.org/10.1016/j.bbi.2017.04.013
Keywords Lipopolysaccharide (LPS),Blood-brain barrier (BBB), High altitude cerebral edema (HACE),Inflammation
Publisher URL http://doi.org/10.1016/j.bbi.2017.04.013

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