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Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity
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MiR-146a negatively regulates dectin-1-induced inflammatory responses.

Leilei Du1, Xu Chen1, Zhimin Duan1

  • 1From Institute of Dermatology, Jiangsu Key Laboratory of Molecular Biology for Skin Diseases and STIs, Chinese Academy of Medical Science and Peking Union Medical College, Nanjing 210042, China.

Oncotarget
|April 29, 2017
PubMed
Summary

MicroRNAs (miRNAs) regulate immunity. This study shows miR-146a, induced by Candida albicans beta-glucan via Dectin-1, suppresses inflammatory cytokines IL-6 and TNFα, acting as a negative feedback regulator.

Keywords:
Candida albicansMiR-146adectin-1inflammatory responsesβ-glucan

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Area of Science:

  • Immunology
  • Molecular Biology
  • Microbiology

Background:

  • Dectin-1 is a key receptor for Candida albicans beta-glucans, initiating innate immune responses.
  • MicroRNAs (miRNAs) are critical regulators of immune cell function, but their role in Dectin-1-mediated inflammation is unclear.
  • Candida albicans is a common human fungal pathogen causing diverse infections.

Purpose of the Study:

  • To investigate the role of miRNAs in the inflammatory response triggered by Dectin-1 activation.
  • To identify specific miRNAs modulated by Candida albicans beta-glucan (CaIG) through the Dectin-1 pathway.
  • To elucidate the functional impact of identified miRNAs on cytokine production and signaling.

Main Methods:

  • THP-1 cells were treated with insoluble beta-glucan from Candida albicans (CaIG).
  • Cytokine (IL-6, TNFα) production was measured.
  • miRNA expression profiling and real-time PCR were performed.
  • Dectin-1, Syk, NF-κB, and p38MAPK pathways were analyzed.
  • miR-146a mimics and luciferase reporter assays were used to assess functional effects.

Main Results:

  • CaIG induced IL-6 and TNFα production via Dectin-1-Syk-NF-κB and p38MAPK pathways.
  • miR-146a, miR-30-5p, and miR-210-3p expression increased in CaIG-treated THP-1 cells.
  • miR-146a expression was sustained and dependent on Dectin-1-Syk-NF-κB/p38MAPK signaling.
  • Overexpression of miR-146a suppressed IL-6 and TNFα production.
  • miR-146a inhibited NF-κB signaling by reducing p-IκBα, p65 translocation, and NF-κB promoter activity.

Conclusions:

  • miR-146a is upregulated by Candida albicans beta-glucan through the Dectin-1 pathway.
  • miR-146a acts as a negative feedback regulator, suppressing Dectin-1-induced inflammatory cytokine production.
  • These findings highlight a novel miRNA-mediated mechanism controlling innate immunity against Candida.