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MicroRNAs Constitute a Negative Feedback Loop in Streptococcus pneumoniae-Induced Macrophage Activation

Kathrin Griss1, Wilhelm Bertrams2, Alexandra Sittka-Stark2

  • 1Institute for Lung Research, German Center for Lung Research, Universities of Giessen and Marburg Lung Center Department of Infectious Diseases and Respiratory Medicine, Charité - Universitätsmedizin Berlin.

The Journal of Infectious Diseases
|March 18, 2016
PubMed

Insights

Streptococcus pneumoniae infection triggers microRNA-146a (miRNA-146a) in human macrophages. This miRNA-146a acts as a negative feedback mechanism, limiting excessive inflammation during pneumococcal pneumonia.

Area of Science:

  • Immunology
  • Molecular Biology
  • Microbiology

Background:

  • Streptococcus pneumoniae is a leading cause of pneumonia with high mortality.
  • Controlling innate immune responses is crucial to prevent organ damage during pneumonia.
  • MicroRNAs (miRNAs) are investigated as potential regulators of host-pathogen interactions.

Purpose of the Study:

  • To investigate the role of miRNAs in regulating host cell activation during pneumococcal infection.
  • To identify specific miRNAs involved in the innate immune response to Streptococcus pneumoniae.
  • To elucidate the regulatory mechanisms of miRNA-146a in pneumococcal pneumonia.

Main Methods:

  • Primary human macrophages were exposed to Streptococcus pneumoniae.
  • Transcriptional changes and miRNA deregulation were analyzed.
  • Computational network analysis identified key miRNA regulators.
  • Toll-like receptor 2 (TLR-2) and MyD88 pathways were investigated.
  • Expression levels of downstream inflammatory mediators were assessed.

Main Results:

  • Pneumococcal infection led to significant deregulation of 10 miRNAs in human macrophages.
  • miRNA-146a was identified as a key regulator of host cell activation.
  • Induction of miRNA-146a depended on bacterial structural integrity and TLR-2/MyD88 signaling.
  • miRNA-146a repressed TLR-2 downstream mediators (IRAK-1, TRAF-6) and inflammatory factors (COX-2, IL-1β).
  • miRNA-146a induction did not require autocrine feedback of IL-1β and TNF-α.

Conclusions:

  • Streptococcus pneumoniae recognition induces a negative feedback loop mediated by miRNA-146a.
  • This miRNA-146a acts to prevent excessive inflammation during pneumococcal infection.
  • miRNA-146a plays a critical role in modulating the innate immune response to pneumococci.
  • Other miRNAs may also contribute to regulating inflammation in pneumococcal pneumonia.
Keywords:
Streptococcus pneumoniaemacrophagesmicroRNA

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