TY - JOUR
T1 - Systemic up-regulation of sTNFR2 and IL-6 in Porphyromonas gingivalis pneumonia in mice
AU - Petelin, Milan
AU - Naruishi, Koji
AU - Shiomi, Nobuyuki
AU - Mineshiba, Junji
AU - Arai, Hideo
AU - Nishimura, Fusanori
AU - Takashiba, Shogo
AU - Murayama, Yoji
N1 - Funding Information:
This work was supported in part by Grant-in-Aid for Scientific Research (14657554 to ST) and The JSPS Postdoctoral Fellowship for Foreign Researchers (P-01761 to YM for MP) form Japan Society for the Promotion of Science.
PY - 2004/2
Y1 - 2004/2
N2 - 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.
AB - 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.
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U2 - 10.1016/j.yexmp.2003.09.002
DO - 10.1016/j.yexmp.2003.09.002
M3 - Article
C2 - 14738872
AN - SCOPUS:0347301680
SN - 0014-4800
VL - 76
SP - 76
EP - 81
JO - Experimental and Molecular Pathology
JF - Experimental and Molecular Pathology
IS - 1
ER -