• Media type: E-Article
  • Title: Specific Modulation of Astrocyte Inflammation by Inhibition of Mixed Lineage Kinases with CEP-1347
  • Contributor: Falsig, Jeppe; Pörzgen, Peter; Lotharius, Julie; Leist, Marcel
  • imprint: The American Association of Immunologists, 2004
  • Published in: The Journal of Immunology, 173 (2004) 4, Seite 2762-2770
  • Language: English
  • DOI: 10.4049/jimmunol.173.4.2762
  • ISSN: 0022-1767; 1550-6606
  • Keywords: Immunology ; Immunology and Allergy
  • Origination:
  • Footnote:
  • Description: <jats:title>Abstract</jats:title> <jats:p>Inflammatory conversion of murine astrocytes correlates with the activation of various MAPK, and inhibition of terminal MAPKs like JNK or p38 dampens the inflammatory reaction. Mixed lineage kinases (MLKs), a family of MAPK kinase kinases, may therefore be involved in astrocyte inflammation. In this study, we explored the effect of the MLK inhibitors CEP-1347 and CEP-11004 on the activation of murine astrocytes by either TNF plus IL-1 or by a complete cytokine mix containing additional IFN-γ. The compounds blocked NO-, PG-, and IL-6 release with a median inhibitory concentration of ∼100 nM. This activity correlated with a block of the JNK and the p38 pathways activated in complete cytokine mix-treated astrocytes. Although CEP-1347 did not affect the activation of NF-κB, it blocked the expression of cyclooxygenase-2 and inducible NO synthase at the transcriptional level. Quantitative transcript profiling of 17 inflammation-linked genes revealed a specific modulation pattern of astrocyte activation by MLK inhibition, for instance, characterized by up-regulation of the anti-stress factors inhibitor of apoptosis protein-2 and activated transcription factor 4, no effect on manganese superoxide dismutase and caspase-11, and down-regulation of major inflammatory players like TNF, GM-CSF, urokinase-type plasminogen activator, and IL-6. In conclusion, MLK inhibitors like CEP-1347 are highly potent astrocyte immune modulators with a novel spectrum of activity.</jats:p>
  • Access State: Open Access