Chronic Morphine Effect on Inflammatory Cytokine Production in Activated BV-2 Microglia Cell Line via Akt/Gsk3β Signaling

The pathophysiology of chronic morphine on the immune system, especially on the cells of the innate immune system that leads to an immune compromise state has not been fully elucidated. The cells of the innate immune system are the first line of defense in mounting an immune response needed in infections, inflammation, cancer development, etc. One of the ways by which these innate immune cells act is by the production of cytokines with direct effects and to also recruit other immune cells, as required. A balance of pro- and anti-inflammatory cytokines is necessary for immune competence. I hypothesized that chronic morphine would act via a classical opioid receptor to stimulate the PI3K/Akt/Gsk3β pathway to produce predominantly anti-inflammatory cytokines. Cytokine gene expression levels were assessed via RT-PCR; Akt and Gsk3β protein levels measured using indirect ELISA. The data suggests that chronic morphine causes a significant reduction in IL-6 production, but does not act via the Akt/Gsk3β pathway or the classical opioid receptor to cause this effect in microglia cells