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Regulation of miRNA transcription in macrophages in response to Candida albicans

Claire E Monk1, György Hutvagner, J Simon C Arthur

  • 1MRC Protein Phosphorylation Unit, College of Life Sciences, Sir James Black Complex, University of Dundee, Dundee, Scotland.

Plos One
|November 10, 2010
PubMed

Insights

MicroRNAs (miRNAs) like miR-146, miR-155, miR-455, and miR-125a are upregulated in macrophages after encountering pathogens or LPS. These miRNAs help regulate inflammatory responses by modulating signaling pathways.

Area of Science:

  • Immunology
  • Molecular Biology
  • RNA Biology

Background:

  • Macrophages utilize pattern recognition receptors (PRRs) to detect pathogens, activating signaling pathways like MAPK and NFκB.
  • These pathways induce pro-inflammatory cytokines crucial for pathogen clearance but require negative feedback to prevent tissue damage.
  • MicroRNAs (miRNAs) are regulatory RNAs that can influence protein expression and potentially modulate PRR signaling pathways.

Purpose of the Study:

  • To identify miRNAs upregulated in mouse macrophages stimulated by heat-killed Candida albicans and lipopolysaccharide (LPS).
  • To investigate the signaling pathways involved in the transcriptional regulation of these upregulated miRNAs.
  • To explore the role of the anti-inflammatory cytokine IL-10 in modulating miRNA expression.

Main Methods:

  • Quantitative analysis of miRNA expression profiles in mouse macrophages.
  • Stimulation of macrophages with heat-killed Candida albicans and LPS.
  • Inhibition of specific signaling pathways (NFκB, ERK1/2, p38 MAPK) to assess their role in miRNA transcription.
  • Treatment with IL-10 to evaluate its effect on miRNA induction.

Main Results:

  • Candida albicans and LPS induced the upregulation of miR-146, miR-155, miR-455, and miR-125a in macrophages.
  • NFκB signaling was essential for the transcription of all four identified pri-miRNAs.
  • ERK1/2 and p38 MAPK pathways were also required for pri-miR-125a transcription.
  • IL-10 induced miR-146a/b but inhibited miR-155 induction.

Conclusions:

  • miR-455, miR-125, miR-146, and miR-155 are key regulators of macrophage function following PRR stimulation.
  • These miRNAs play a role in the negative feedback mechanisms controlling inflammatory responses.
  • Understanding these miRNA regulatory networks is crucial for controlling excessive inflammation in response to pathogens.

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