β-adrenoceptor mediated surgery-induced production of pro-inflammatory cytokines in rat microglia cells

Immunological changes initiated by major operative injury may result in inflammatory responses in both peripheral and central nervous system, which may lead to organ dysfunction. Recent studies indicate that β-adrenergic receptors (β-ARs) may mediate production of pro-inflammatory cytokines in the brain. In the present study propranolol (β-AR antagonist), but not prazosin (α1-AR antagonist), antagonized surgical trauma induced pro-inflammatory cytokine production in microglia cells isolated from rats. β-AR activation in the absence of pro-inflammatory stimuli increased IL-1β, TNF-α and IL-6 mRNA and protein expressions in the primary microglia cell culture. Isoproterenol (β-AR agonist) treatment induced a time- and concentration-dependent increase of IL-1β in cells. Both ERK1/2 and P38 MAPK inhibitor, but not PKA and JNK1/2 inhibitor abrogated isoproterenol-induced IL-1β and IL-6 production in microglia cells. In conclusion, the results suggest that β-ARs possess pro-inflammatory properties by modulating the functions of microglia cell.