Source:http://linkedlifedata.com/resource/pubmed/id/14738872
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2004-1-23
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| pubmed:abstractText |
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.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor...,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor...,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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| pubmed:status |
MEDLINE
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| pubmed:month |
Feb
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| pubmed:issn |
0014-4800
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
76
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
76-81
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:14738872-Animals,
pubmed-meshheading:14738872-Antigens, CD,
pubmed-meshheading:14738872-Bacteroidaceae Infections,
pubmed-meshheading:14738872-Disease Models, Animal,
pubmed-meshheading:14738872-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:14738872-Interleukin-1,
pubmed-meshheading:14738872-Interleukin-6,
pubmed-meshheading:14738872-Lung,
pubmed-meshheading:14738872-Male,
pubmed-meshheading:14738872-Mice,
pubmed-meshheading:14738872-Mice, Nude,
pubmed-meshheading:14738872-Pneumonia, Aspiration,
pubmed-meshheading:14738872-Porphyromonas gingivalis,
pubmed-meshheading:14738872-Receptors, Tumor Necrosis Factor,
pubmed-meshheading:14738872-Receptors, Tumor Necrosis Factor, Type I,
pubmed-meshheading:14738872-Receptors, Tumor Necrosis Factor, Type II,
pubmed-meshheading:14738872-Tumor Necrosis Factor-alpha,
pubmed-meshheading:14738872-Up-Regulation
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| pubmed:year |
2004
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| pubmed:articleTitle |
Systemic up-regulation of sTNFR2 and IL-6 in Porphyromonas gingivalis pneumonia in mice.
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| pubmed:affiliation |
Department of Pathophysiology-Periodontal Science, Okayama University Graduate School of Medicine and Dentistry, Okayama 700-8525, Japan.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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