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IL-10 suppresses LPS-induced KC mRNA expression via a translation-dependent decrease in mRNA stability

H S Kim1, D Armstrong, T A Hamilton

  • 1Department of Immunology, Lerner Research Institute, Cleveland Clinic Foundation, Ohio 44195, USA.

Journal of Leukocyte Biology
|July 17, 1998
PubMed
Summary
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Interleukin-10 (IL-10) suppresses KC chemokine gene expression in macrophages by decreasing mRNA stability, not transcription. This IL-10 effect requires ongoing protein synthesis, indicating a complex regulatory mechanism.

Area of Science:

  • Immunology
  • Molecular Biology
  • Gene Regulation

Background:

  • Interleukin-10 (IL-10) is a key immunosuppressive cytokine.
  • Chemokines, like KC, play crucial roles in inflammatory responses.
  • Understanding IL-10's regulatory mechanisms on chemokine gene expression is vital for controlling inflammation.

Purpose of the Study:

  • To elucidate the mechanism by which IL-10 suppresses KC chemokine gene expression in mouse macrophages.
  • To determine if IL-10 affects KC gene transcription or mRNA stability.
  • To investigate the role of protein synthesis in IL-10-mediated suppression.

Main Methods:

  • Treatment of mouse macrophages with lipopolysaccharide (LPS) and varying concentrations/timing of IL-10.
  • Measurement of KC mRNA levels over time.

Related Experiment Videos

  • Assessment of KC gene transcription rates and mRNA stability.
  • Inhibition of protein synthesis using specific inhibitors.

    • Main Results:

    • IL-10 suppressed KC mRNA levels late in the LPS response.
    • IL-10 decreased KC mRNA stability without affecting gene transcription.
    • The suppressive effect of IL-10 was abrogated by protein synthesis inhibitors, even when added post-LPS/IL-10 exposure.

    Conclusions:

    • IL-10-mediated suppression of KC gene expression occurs at the post-transcriptional level by destabilizing KC mRNA.
    • This destabilization process is dependent on coincident KC mRNA translation, implying a requirement for newly synthesized proteins.
    • The findings reveal a novel mechanism for IL-10 in regulating inflammatory gene expression.