Submission Date

7-22-2021

Document Type

Paper- Restricted to Campus Access

Department

Neuroscience

Faculty Mentor

Jennifer King

Comments

Presented during the 23rd Annual Summer Fellows Symposium, July 23, 2021 at Ursinus College.

Project Description

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 injury or infection. Neuroinflammation typically occurs as a result of infection or injury and initiates the activation of microglial cells. The impact of neuroinflammation is observable in many neurodegenerative disorders such as Parkinson’s Disease, Alzheimer’s Disease, traumatic brain injury, and other neurological diseases. While beneficial for health and repair, neuroinflammation, when long term, can be counterproductive and instead prove detrimental to CNS health by over-activating phagocytes. Upon activation, microglial cells clear cellular debris and pathogens by engulfing, through a process recognized as phagocytosis. We previously have found that the HIV-Trans-Activator of Transcription (Tat) protein, a neuroinflammatory protein, induces a decrease in phagocytic activity of BV-2 cells, an immortalized microglial cell line. We also use lipopolysaccharide (LPS), a neurotoxin known to increase neuroinflammation. Here we further observe the effects of HIV-Tat and LPS -induced neuroinflammation on the phagocytic activity of BV-2 cells over 30 minutes, 1-, 2-, and 24-hour time courses.

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