title: Systemic up-regulation of sTNFR2 and IL-6 in Porphyromonas gingivalis pneumonia in mice.
abstract: 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)-alpha, interleukin-6 (IL-6), and IL-1beta production in both lung tissue and serum. We also elucidated production of soluble (s) TNF receptor (R) s, because TNF-alpha is considered to be a dominant inflammatory mediator. Lung TNF-alpha levels significantly increased at 2 h after infection, and rapidly returned to basal level at 24 h. Consistent with increase of TNF-alpha, 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-1beta 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-alpha in Pg-induced lung inflammation simulated aspiration pneumonia.
authors.affiliation: Department of Pathophysiology-Periodontal Science, Okayama University Graduate School of Medicine and Dentistry, Okayama 700-8525, Japan.
authors.forename: Milan
authors.initials: M
authors.lastname: Petelin
authors.forename: Koji
authors.initials: K
authors.lastname: Naruishi
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Shiomi
authors.forename: Junji
authors.initials: J
authors.lastname: Mineshiba
authors.forename: Hideo
authors.initials: H
authors.lastname: Arai
authors.forename: Fusanori
authors.initials: F
authors.lastname: Nishimura
authors.forename: Shogo
authors.initials: S
authors.lastname: Takashiba
authors.forename: Yoji
authors.initials: Y
authors.lastname: Murayama
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000378:metabolism*; D016866:Bacteroidaceae Infections / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D007375:Interleukin-1 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism*; D008168:Lung / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D008819:Mice, Nude; D011015:Pneumonia, Aspiration / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D016966:Porphyromonas gingivalis / Q000472:pathogenicity / Q000502:physiology*; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism*; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D015854:Up-Regulation
chemical_list: D015703:Antigens, CD; D007375:Interleukin-1; D015850:Interleukin-6; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D014409:Tumor Necrosis Factor-alpha