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Mycoplasma pneumoniae MPN606 induces inflammation by activating MAPK and NF-κB signaling pathways

Ru Zhang1, Yingying Zuo1, Shuihong Li1

  • 1Institute of Pathogenic Biology, Hengyang Medical College, University of South China, 421001, Hengyang, Hunan, China.

Microbial Pathogenesis
|January 13, 2025
PubMed

Insights

Mycoplasma pneumoniae MPN606 protein triggers macrophage activation and inflammation. It activates NF-κB and MAPK pathways, leading to pro-inflammatory cytokine release in community-acquired pneumonia.

Area of Science:

  • Immunology
  • Microbiology
  • Molecular Biology

Background:

  • Mycoplasma pneumoniae is a key cause of community-acquired pneumonia (CAP).
  • The precise pathogenic mechanisms of M. pneumoniae, particularly its role in inflammation, require further elucidation.
  • Inflammatory responses are central to CAP pathology.

Purpose of the Study:

  • To investigate the inflammatory role of the M. pneumoniae MPN606 protein.
  • To explore the molecular mechanisms underlying MPN606-induced inflammation.

Main Methods:

  • Stimulation of RAW264.7 macrophage cells with recombinant MPN606 (rMPN606).
  • Measurement of nitric oxide (NO), TNF-α, and IL-6 levels.
  • Analysis of iNOS, IL-6, and TNF-α mRNA expression.
  • Western blot analysis for iNOS, p65, p38, and ERK phosphorylation.
  • Cellular immunofluorescence to track NF-κB translocation.

Main Results:

  • rMPN606 induced NO release and increased TNF-α and IL-6 cytokine expression.
  • Upregulation of iNOS, IL-6, and TNF-α mRNA was observed.
  • rMPN606 enhanced iNOS protein expression and phosphorylation of p65, p38, and ERK.
  • NF-κB nuclear translocation was significantly increased in rMPN606-stimulated cells.

Conclusions:

  • Mycoplasma pneumoniae MPN606 protein induces M1-type macrophage activation.
  • MPN606 promotes pro-inflammatory factor secretion via activation of NF-κB and MAPK signaling pathways.
Keywords:
M. pneumoniaeMAPKNF-κBRAW264.7rMPN606

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