Glia
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Cytokines play an important role in the onset, regulation, and propagation of immune and inflammatory responses within the central nervous system (CNS). The main source of cytokines in the CNS are microglial cells. Under inflammatory conditions, microglial cells are capable of producing pro- and antiinflammatory cytokines, which convey essential impact on the glial and neuronal environment. ⋯ Under these conditions, i.e., incubation with the inflammatory cytokines and the high fraction of microglia (M30), microglial cells revealed a significant increase of activated round phagocytotic cells accompanied by a reduction of astroglial connexin 43 (Cx43) expression, a reduced functional coupling together with depolarization of the membrane resting potential (MRP). When the antiinflammatory mediator TGF-beta1 was added to proinflammatory altered M30 cocultures, a reversion of microglial activation and reconstitution of functional coupling together with recovery of the astroglial MRP was achieved. Finally IFN-beta, added to M5 cocultures was able to prevent the effects of the proinflammatory cytokines TNF-alpha, IL-1beta, and IFN-gamma.