Submission Date


Document Type

Paper- Restricted to Campus Access



Faculty Mentor

Jennifer King


Presented during the 21st Annual Summer Fellows Symposium, July 19, 2019 at Ursinus College.

Project Description

Neuroinflammatory response is a host-defense mechanism that helps to protect and restore normal cell structure and function of the brain against injury and infections (More et al. 2013). In neurodegenerative diseases, neuroinflammation first clears the infection that helps to control neurodegenerative disease severity or progression (Kempuraj et al. 2017). However, persistent neuroinflammation can increase neurodegeneration in the central nervous system (CNS) (Kempuraj et al. 2017). Microglia, which are brain resident macrophages, aid in the immune response in the CNS and when infected with HIV, they can release pro-inflammatory cytokines. These cytokines can create an inflamed and toxic environment surrounding the neurons. Activation of microglia induces their proliferation in neuroinflammatory conditions (Perry et al., 2010; Perry, 2016). Over activated microglia can lead to alterations in their cytoskeleton thereby effecting functional activity. Cofilin and Phospho-Cofilin (P-Cofilin) are regulatory proteins that assist in actin reorganization and cytoskeletal function. We used HIV-Tat protein as a model inflammatory mediator to observe how microglial cells respond to an inflamed environment. We hypothesize that inflammatory mediators like HIV-Tat will result in a dysregulation of Cofilin and P- Cofilin expression leading to subsequent alterations in phagocytotic activity. This could lead to direct damage of the microglia skeleton, inhibiting its activity in immune responses and indirect neuronal death.