Systemic up-regulation of sTNFR2 and IL-6 in Porphyromonas gingivalis pneumonia in mice

Milan Petelin, Koji Naruishi, Nobuyuki Shiomi, Junji Mineshiba, Hideo Arai, Fusanori Nishimura, Shogo Takashiba, Yoji Murayama

Research output: Contribution to journalArticlepeer-review

15 Citations (Scopus)


Aspiration pneumonia is a common cause of death in older people, and the pathophysiology is a chronic respiratory failure with a mild airway inflammation. In this study, we established a mild inflammatory pneumonia model using Porphyromonas gingivalis (Pg) pathogen-infected mice. It elucidated the effects of Pg-infected pneumonia on proinflammatory cytokines tumor necrosis factor (TNF)-α, interleukin-6 (IL-6), and IL-1β production in both lung tissue and serum. We also elucidated production of soluble (s) TNF receptor (R) s, because TNF-α is considered to be a dominant inflammatory mediator. Lung TNF-α levels significantly increased at 2 h after infection, and rapidly returned to basal level at 24 h. Consistent with increase of TNF-α, remarkable increase of sTNFR2 but not sTNFR1 was detected in lung tissue from 2 to 72 h. Interestingly, sTNFR2/sTNFR1 ratio was significantly enhanced at 2 h in serum. In addition, lung IL-1β and IL-6 levels also significantly increased from 2 to 24 h. Importantly, we found that IL-6 levels in serum reflected its local level. These results may suggest that systemically produced sTNFR2 and IL-6 could be a key role to modulate proinflammatory activities of TNF-α in Pg-induced lung inflammation simulated aspiration pneumonia.

Original languageEnglish
Pages (from-to)76-81
Number of pages6
JournalExperimental and Molecular Pathology
Issue number1
Publication statusPublished - Feb 2004


  • Aspiration pneumonia
  • IL-1β
  • IL-6
  • Porphyromonas gingivalis
  • TNF-α
  • sTNFR1
  • sTNFR2

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Molecular Biology
  • Clinical Biochemistry


Dive into the research topics of 'Systemic up-regulation of sTNFR2 and IL-6 in Porphyromonas gingivalis pneumonia in mice'. Together they form a unique fingerprint.

Cite this