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Cytosolic mtDNA released from pneumolysin-damaged mitochondria triggers IFN-β production in epithelial cells

Yuting Fang1, Xuemei Zhang1, Chang Lu1

  • 1School of Laboratory Medicine, Key Laboratory of Diagnostic Medicine Designated by the Ministry of Education, Chongqing Medical University, Chongqing 400016, People's Republic of China.

Canadian Journal of Microbiology
|March 20, 2020
PubMed

Insights

Pneumolysin (Ply) from Streptococcus pneumoniae damages mitochondria, releasing DNA that triggers interferon-beta (IFN-β) in lung epithelial cells. This study reveals a key mechanism in the host

Area of Science:

  • Immunology
  • Cell Biology
  • Microbiology

Background:

  • Pneumolysin (Ply) is a key virulence factor of Streptococcus pneumoniae.
  • Previous studies linked Ply-induced interferon-beta (IFN-β) in macrophages to mitochondrial DNA (mtDNA) release.
  • Human bronchial epithelial cells (BEAS-2B) are crucial at the airway's inflammatory interface.

Purpose of the Study:

  • To investigate the role of Ply in inducing IFN-β expression in human bronchial epithelial cells.
  • To determine if mitochondrial damage and subsequent mtDNA release mediate this response.
  • To elucidate the mechanism of epithelial cell response to S. pneumoniae infection.

Main Methods:

  • Exposure of BEAS-2B cells to purified Ply.
  • Assessment of IFN-β expression.
  • Evaluation of mitochondrial damage and mtDNA release in vitro and in vivo (mouse infection model).

Main Results:

  • Purified Ply induced significant IFN-β expression in human epithelial cells.
  • Ply exposure caused observable mitochondrial damage in both in vitro and in vivo models.
  • Increased mtDNA concentrations were detected in bronchial lavage fluid of infected mice, correlating with infection.

Conclusions:

  • Ply triggers IFN-β production in epithelial cells.
  • This epithelial response is mediated by mtDNA released from Ply-damaged mitochondria.
  • The study highlights a significant mechanism of epithelial cell modulation of the IFN-β response to S. pneumoniae.
Keywords:
ADNmtIFN-βcellules épithélialesdommage mitochondrialepithelial cellsmitochondrial damagemtDNApneumolysin (Ply)pneumolysine (Ply)

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