Date Presented

Spring 5-18-2025

Document Type

Thesis

First Advisor

Dr. David Freier

Second Advisor

Dr. Ei Hlaing

Third Advisor

Dr. Price Blair

Abstract

Neuroinflammation is a complex synergy of different cells within the central nervous system. Astrocytes play a key role in the maintenance of neural functioning, but take a special part in the inflammatory process as well. By releasing pro-inflammatory modulators like cytokines, chemokines, and reactive oxygen species, astrocytes modulate the inflammatory response in the brain. Astrocytes can be activated into this proinflammatory state in response to pathogen derived molecules such as bacterial lipopolysaccharides (LPS). Lipopolysaccharides are glycoproteins derived from gram negative bacteria and commonly used to stimulate cells in vitro to produce an inflammatory response. To look at the effects of LPS on astrocyte inflammation, C8-D1a neonatal murine astrocytes were stimulated dose responsively from 0-1000ng/mL. No significant change in nitric oxide production as measured by the Greiss reaction or in the pro-inflammatory cytokine TNF-alpha was observed through multiple trials. These results are inconsistent within the published literature on astrocyte inflammation, thus more exploration is necessary to deduce the true effects of bacterial stimulation on astrocyte inflammatory responses.

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