METHAMPHETAMINE INDUCED IMMUNE DYSREGULATION
Methamphetamine (METH) use can induce and contribute to the development of neurodegenerative disorders. In this study, we evaluated the roles of specific cytokines in the pathology of acute and chronic methamphetamine usage in vitro and in vivo. An immortalized rat astrocyte CTX-TNA2 cell line was used for a model of immune cells in central nervous system. Cells were treated with methamphetamine hydrochloride, dopamine hydrochloride as a reference point, and lipopolysaccharides (LPS) as a model of immunogenic stimulant. Our in vivo experimental design utilized female NIH-swiss mice that underwent a seven-day treatment period. The control mice were administrated 0.9% saline, and our treated mice were administrated 12 mg/kg of (+)- methamphetamine through intraperitoneal injections. Cells and tissue specific gene expression of key signal transducers, cytokines, and their receptors were evaluated with qPCR. Systemic cytokine levels were evaluated with flow-cytometry. The results suggest that METH acts locally to the brain tissue to cause a shift toward inflammation by increasing cytokine, receptor and signal transducer of interleukin-6 (IL-6) and interleukin-17 (IL-17) pathways. While suppressing systemic cytokine production leading to an imbalance in Th-X paradigm.