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CANNABINOIDS DELTA-9-TETRAHYDROCANNABINOL (THC) AND CP55,940 ABLATE SPECIFIC CHEMOKINE AND CYTOKINE INFLAMMATORY RESPONSE IN BV-2 MOUSE MICROGLIAL CELLS ACTIVATED WITH HIV-1 PRO-INFLAMMATORY PROTEIN TAT

Despite the widespread use of Highly Active Anti-retroviral Therapy (HAART) to combat Human Immunodeficiency Virus (HIV), the causative agent of acquired immunodeficiency syndrome (AIDS), HIV-Associated Neurocognitive Disorders (HANDs) still remain a dire issue. HIV can enter the brain through infected monocytes and infect microglia, the resident macrophages within that compartment. Due to its pro-inflammatory properties, HIV regulatory protein Tat (Transactivating protein) may play a role in the progression of neurocognitive disorders. The aim of this project was to determine whether the select cannabinoids THC and CP55,940 could ablate the inflammatory response on BV-2 mouse microglia cells caused by Tat. Within the constraints of the experiment, no major effects of cannabinoid treatment were observed at the level of the proteome as tested by two-dimensional gel electrophoresis . In contrast, these cannabinoids ablated the inflammatory response caused by the HIV protein Tat at the level of the secretome and at the level of gene expression. These collective observations suggest that select cannabinoids have the potential to down-regulate the elicitation of proinflammatory gene products that are engendered by the HIV protein Tat. Furthermore, the results suggest a potential for cannabinoid agonists at cannabinoid receptors to serve as adjunct ablative agents in the treatment of HIV-associated neuropathological processes.

Identiferoai:union.ndltd.org:vcu.edu/oai:scholarscompass.vcu.edu:etd-1544
Date25 June 2013
CreatorsMaddux, Rebecca
PublisherVCU Scholars Compass
Source SetsVirginia Commonwealth University
Detected LanguageEnglish
Typetext
Formatapplication/pdf
SourceTheses and Dissertations
Rights© The Author

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