Chronic Microglial Activation After an Inflammatory Event

Systemic lipopolysaccharide (LPS)-induced microglial activation results in different temporal reduction of CD200 and CD200 receptor gene expression in the brain.

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Systemic lipopolysaccharide (LPS)-induced microglial activation results in different temporal reduction of CD200 and CD200 receptor gene expression in the brain.

J Neuroimmunol. 2009 Sep 29;214(1-2):78-82

Authors: Masocha W

LPS activates microglia, which are normally maintained in a quiescent state by CD200-CD200 receptor (CD200R) interaction.

MAC-1 (a microglia marker) mRNA expression was increased in mice brains up to 1 year post LPS administration (i.p.). Minocycline treatment did not prevent LPS (5 mg/kg)-induced increase in MAC-1 mRNA but reduced that induced by 0.1 mg/kg LPS. CD200R mRNA decreased starting at 4 h, whereas CD200 mRNA increased at 4 h and decreased at 1 year post LPS inoculation.

Thus, LPS-induced changes in CD200-CD200R equilibrium might keep microglia chronically activated. Minocycline does not effectively inhibit microglia activation induced by high-dose LPS.

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This article demonstrates that chronic microglial activation can occur via a single inflammatory event. Microglial activation producing pro-inflammatory cytokines is one of the pathophysiologies behind a diverse group of illnesses including mood disorders and other mental illnesses, fibromyalgia, sickness behaviors in response to infection, migraine, other inflammatory conditions, etc.

LPS is a substance used in psychoimmunology studies to induce a pro-inflammatory immune response. When instroduced into the gastrointestinal system, it activates the sympathetic nervous system via vagal sensory neurons, which monitor for the presence of pro-inflammatory cytokines.

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