Abstract | BACKGROUND: METHODS: RESULTS: Lung neutrophil accumulation and microvascular permeability were significantly increased after unresuscitated HS, meanwhile, lung interleukin-1beta and tumor necrosis factor-alpha were gradually augmented. TLR4 mRNA, TLR4 distribution and TLR4 protein were also significantly increased in TLR4 wt mice, however, no above-mentioned changes appeared in TLR4 mutant mice. CONCLUSIONS: TLR4 is strongly associated with the pathogenesis of ALI induced by unresuscitated HS, which may serve as a useful therapeutic target.
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Authors | Tangfeng Lv, Xiaokun Shen, Yi Shi, Yong Song |
Journal | The Journal of trauma
(J Trauma)
Vol. 66
Issue 1
Pg. 124-31
(Jan 2009)
ISSN: 1529-8809 [Electronic] United States |
PMID | 19131815
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Interleukin-1
- Lipopolysaccharides
- Lymphotoxin-alpha
- Tlr4 protein, mouse
- Toll-Like Receptor 4
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Topics |
- Acute Lung Injury
(etiology, metabolism)
- Analysis of Variance
- Animals
- Blotting, Western
- Immunoenzyme Techniques
- Interleukin-1
(metabolism)
- Lipopolysaccharides
- Lymphotoxin-alpha
(metabolism)
- Male
- Mice
- Mice, Inbred Strains
- Random Allocation
- Reverse Transcriptase Polymerase Chain Reaction
- Shock, Hemorrhagic
(complications, metabolism)
- Toll-Like Receptor 4
(metabolism)
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