A single dose of trichloroethylene given during development does not substantially alter markers of neuroinflammation in brains of adult mice

Abstract

Trichloroethylene (TCE) is a widespread environmental contaminant associated with developmental immu- notoxicity and neurotoxicity. Previous studies have shown that MRLþ/þ mice exposed to TCE from gesta- tion through early-life demonstrate robust increases in inflammatory markers in peripheral CD4þ T-cells, as well as glutathione depletion and increased oxidative stress in cerebellum-associated with alterations in behavior. Since increased oxidative stress is associated with neuroinflammation, we hypothesized that neuroinflammatory markers could be altered relative to unexposed mice. MRLþ/þ mice were given 0.5mg/ml of TCE in vehicle or vehicle (water with 1% Alkamuls EL-620) from conception through early adulthood via drinking water to dams and then directly to post-weaning offspring. Animals were euthan- ized at 49days of age and levels of pro- and anti-inflammatory cytokines, density of T-cell staining, and micro-glial morphology were evaluated in brains to begin to ascertain a neuroinflammatory profile. Levels of IL-6 were decreased in female animals and while not statistically significant, and levels of IL-10 were higher in brains of exposed male and female animals. Supportive of this observation, although not statis- tically significant, the number of ameboid microglia was higher in exposed relative to unexposed animals. This overall profile suggests the emergence of an anti-inflammatory/neuroprotective phenotype in exposed animals, possibly as a compensatory response to neuroinflammation that is known to be induced by developmental exposure to TCE.