Streptococcus pneumoniae induces human β-defensin-2 and -3 in human lung epithelium

Exp Lung Res. 2012 Mar;38(2):100-10. doi: 10.3109/01902148.2011.652802.


Streptococcus pneumoniae is an important causative agent of pneumonia in humans. Pulmonary epithelial surfaces constitutes not only a mechanical barrier against invading pathogens but also essentially contribute to innate immunity by producing antimicrobial peptides such as human β-defensin-2 (hBD-2) and -3 (hBD-3). In this study the authors demonstrated that pneumococci induced hBD-2 and hBD-3 expression in human pulmonary epithelial cells. Further analysis indicated an essential role of Toll-like receptor 2 (TLR2) for the expression of both peptides in infected pulmonary epithelial cells. Whereas the hBD-2 release was controlled by the phosphoinositide 3-kinase (PI3K) and the transcription factor nuclear factor kappa B (NF-κB), hBD-3 was triggered via the c-Jun N-terminal kinase (JNK)-activator protein 1 (AP-1) pathway. Additionally, the authors showed that exogenous hBD-2 as well as hBD-3 elicited a strong antimicrobial effect on S. pneumoniae. Thus, differential regulation of the expression of hBD-2 and hBD-3 might play an important role in pneumococci pneumonia.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alveolar Epithelial Cells / immunology
  • Alveolar Epithelial Cells / metabolism
  • Alveolar Epithelial Cells / microbiology*
  • Humans
  • Immunity, Innate
  • Lung / immunology
  • Lung / metabolism
  • Lung / microbiology*
  • NF-kappa B / metabolism
  • Phosphatidylinositol 3-Kinase / metabolism
  • Proto-Oncogene Proteins c-jun / metabolism
  • Streptococcus pneumoniae / immunology
  • Streptococcus pneumoniae / pathogenicity*
  • Toll-Like Receptor 2 / metabolism
  • Transcription Factor AP-1 / metabolism
  • beta-Defensins / biosynthesis*


  • DEFB103A protein, human
  • DEFB4A protein, human
  • NF-kappa B
  • Proto-Oncogene Proteins c-jun
  • TLR2 protein, human
  • Toll-Like Receptor 2
  • Transcription Factor AP-1
  • beta-Defensins
  • Phosphatidylinositol 3-Kinase