INTERLEUKIN 1 OF THE CENTRAL NERVOUS SYSTEM IS PRODUCED BY AMEBOID MICROGLIA

INTERLEUKIN 1 OF THE CENTRAL NERVOUS SYSTEM IS PRODUCED BY AMEBOID MICROGLIA

Volume 164 August 1986 594–604 | BY DANA GIULIAN,* TIMOTHY J. BAKER,* LI-CHEN N. SHIH,‡ AND LAWRENCE B. LACHMAN‡
The study by Giulian et al. investigates the role of interleukin 1 (IL-1) in the central nervous system (CNS), focusing on its production by ameboid microglia. The authors demonstrate that ameboid microglia, when activated, release significant quantities of IL-1, which is an 18 kD peptide with biological activity. This IL-1 is identical to that released by macrophages and can be neutralized by anti-murine IL-1 antibodies. The study also shows that microglial IL-1 stimulates the proliferation of astroglia in vitro, increasing the number of GFAP-positive astroglia by five to sevenfold and enhancing [³H]-thymidine incorporation by three to fivefold. The authors propose that IL-1 released from activated microglial cells may regulate astroglial proliferation during brain injury or development. They suggest that ameboid microglia are the primary source of brain IL-1 in vitro, and that this factor may play a crucial role in controlling glial outgrowth and reducing glial scarring. The findings highlight the potential of IL-1 as a marker for microglial activation and its significance in monitoring degenerative or inflammatory diseases of the CNS.The study by Giulian et al. investigates the role of interleukin 1 (IL-1) in the central nervous system (CNS), focusing on its production by ameboid microglia. The authors demonstrate that ameboid microglia, when activated, release significant quantities of IL-1, which is an 18 kD peptide with biological activity. This IL-1 is identical to that released by macrophages and can be neutralized by anti-murine IL-1 antibodies. The study also shows that microglial IL-1 stimulates the proliferation of astroglia in vitro, increasing the number of GFAP-positive astroglia by five to sevenfold and enhancing [³H]-thymidine incorporation by three to fivefold. The authors propose that IL-1 released from activated microglial cells may regulate astroglial proliferation during brain injury or development. They suggest that ameboid microglia are the primary source of brain IL-1 in vitro, and that this factor may play a crucial role in controlling glial outgrowth and reducing glial scarring. The findings highlight the potential of IL-1 as a marker for microglial activation and its significance in monitoring degenerative or inflammatory diseases of the CNS.
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