Document Type

Paper- Restricted to Campus Access

Publication Date


Faculty Mentor

Jennifer King


Microglia, the resident macrophage of the Central Nervous System (CNS), play a primary role in maintaining the health of the CNS through its immune response to neuroinflammation, which occurs as a result of injury or infection. When activated, their phagocytic properties allow them to remove cellular debris, toxins, and damaged cells while also being able to release both pro- and anti-inflammatory cytokines. These properties of Microglia have been studied and correlated with the neural tissue degradation of neurodegenerative diseases such as Alzheimer’s Disease (AD), Parkinson’s Disease (PD), Amyotrophic Lateral Sclerosis (ALS), and Multiple Sclerosis (MS). While beneficial for health and repair, neuroinflammation, when long term, can be counterproductive as overactive pro-inflammatory responses resulting in the phagocytosis of healthy tissue has been observed. Previously our lab found that HIV-Tat, a neuroinflammatory protein, induces a decrease in phagocytic activity of BV-2 cells, an immortalized microglial cell line. We have continued our research with the goal of assessing the effects of neurotoxic protein exposure over time. Here we observe the effects of HIV-Tat and lipopolysaccharide (LPS) -induced neuroinflammation on the phagocytic activity of BV-2 cells over 1-, 12-, and 24-hour time courses.


Presented as part of the Ursinus College Celebration of Student Achievement (CoSA) held April 22, 2021.

The downloadable file is a poster presentation with audio commentary.


Available to Ursinus community only.