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The Journal of Immunology, 1999, 162: 1701-1706.
Copyright © 1999 by The American Association of Immunologists

Negative Feedback Between Prostaglandin and {alpha}- and ß-Chemokine Synthesis in Human Microglial Cells and Astrocytes1

Nazila Janabi2,3, Isabelle Hau and Marc Tardieu

Laboratory of Virus, Neuron and Immunity, Unité de Formation et de Recherche, Kremlin Bicêtre, University of Paris-South, Paris, France

The understanding of immune surveillance and inflammation regulation in cerebral tissue is essential in the therapy of neuroimmunological disorders. We demonstrate here that primary human glial cells were able to produce {alpha}- and ß-chemokines (IL-8 > growth related protein {alpha} (GRO{alpha}) >> RANTES > microphage inflammatory protein (MIP)-1{alpha} and MIP-1ß) in parallel to PGs (PGE2 and PGF2{alpha}) after proinflammatory cytokine stimulation: TNF-{alpha} + IL-1ß induced all except RANTES, which was induced by TNF-{alpha} + IFN-{gamma}. Purified cultures of astrocytes and microglia were also induced by the same combination of cytokines, to produce all these mediators except MIP-1{alpha} and MIP-1ß, which were produced predominantly by astrocytes. The inhibition of PG production by indomethacin led to a 37–60% increase in RANTES, MIP-1{alpha}, and MIP-1ß but not in GRO{alpha} and IL-8 secretion. In contrast, inhibition of IL-8 and GRO activities using neutralizing Abs resulted in a specific 6-fold increase in PGE2 but not in PGF2{alpha} production by stimulated microglial cells and astrocytes, whereas Abs to ß-chemokines had no effect. Thus, the production of PGs in human glial cells down-regulates their ß-chemokine secretion, whereas {alpha}-chemokine production in these cells controls PG secretion level. These data suggest that under inflammatory conditions, the intraparenchymal production of PGs could control chemotactic gradient of ß-chemokines for an appropriate effector cell recruitment or activation. Conversely, the elevated intracerebral {alpha}-chemokine levels could reduce PG secretion, preventing the exacerbation of inflammation and neurotoxicity.




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