The effect of recombinant interleukin-10/Fc fusion protein on lipopolysaccharide-induced acute lung injury in mice

OBJECTIVE: To clarify the regulatory role and mechanism of recombinant interleukin-10/Fc (rIL-10/Fc) fusion protein on inflammatory parameters during development of acute lung injury (ALI) induced by lipopolysaccharide (LPS) in a murine model

Bibliographische Detailangaben
Veröffentlicht in:Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue. - 1998. - 20(2008), 8 vom: 08. Aug., Seite 461-4
1. Verfasser: Bi, Ming-hua (VerfasserIn)
Weitere Verfasser: Wang, Bao-en, Zheng, Xin-xiao, Li, Min, Mayer, Konstantin, Zhang, Shu-wen
Format: Aufsatz
Sprache:Chinese
Veröffentlicht: 2008
Zugriff auf das übergeordnete Werk:Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue
Schlagworte:English Abstract Journal Article Research Support, Non-U.S. Gov't Interleukin-1beta Lipopolysaccharides Recombinant Fusion Proteins Tumor Necrosis Factor-alpha Interleukin-10 130068-27-8 Peroxidase EC 1.11.1.7
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100 1 |a Bi, Ming-hua  |e verfasserin  |4 aut 
245 1 4 |a The effect of recombinant interleukin-10/Fc fusion protein on lipopolysaccharide-induced acute lung injury in mice 
264 1 |c 2008 
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500 |a Citation Status MEDLINE 
520 |a OBJECTIVE: To clarify the regulatory role and mechanism of recombinant interleukin-10/Fc (rIL-10/Fc) fusion protein on inflammatory parameters during development of acute lung injury (ALI) induced by lipopolysaccharide (LPS) in a murine model 
520 |a METHODS: An ALI model was reproduced by intra-tracheal injection of LPS. rIL-10/Fc was administered intraperitoneally. One hundred and thirty-two BALB/c mice were divided into four groups, including saline control group, rIL-10/Fc control group, ALI model group, and rIL-10/Fc treatment group. Twenty-four-hour survival rate was determined in 25 mice of each group. The number of inflammatory cells and inflammatory mediators in bronchial-alveolar lavage fluid (BALF), tumor necrosis factor-alpha (TNF-alpha) and IL-1 beta, and also lung myeloperoxidase (MPO) activity, lung wet/dry (W/D) ratio were determined in the rest of mice. Pathological changes in lung were examined with hematoxylin-eosin (HE) staining, and inflammatory change was evaluated under microscope 
520 |a RESULTS: Levels of TNF-alpha and IL-1 beta in BALF were substantially increased 4 hours after intra-tracheal LPS (both P<0.01), and they were lowered but without significant difference after rIL-10/Fc administration. However, rIL-10/Fc fusion protein markedly attenuated release of TNF-alpha at 8 hours and 12 hours, and IL-1 beta was lowered at 12 hours after LPS challenge. Pre-treatment with rIL-10/Fc fusion protein significantly improved survival rate at 24 hours in LPS challenged mice (P<0.01). There was no significant difference in cell count in BALF, MPO, lung W/D ratio, after treatment of rIL-10/Fc fusion protein. Obvious inflammatory changes were found in lung was found pathologically at 24 hours after LPS injection, but there was no significant difference compared with ALI mice with rIL-10/Fc fusion protein administration 
520 |a CONCLUSION: rIL-10/Fc fusion protein inhibits release of TNF-alpha and IL-1 beta in BALF in a LPS-induced ALI murine model. rIL-10/Fc fusion protein improves survival rate in ALI mice by decreasing the release of pro-inflammatory cytokines 
650 4 |a English Abstract 
650 4 |a Journal Article 
650 4 |a Research Support, Non-U.S. Gov't 
650 7 |a Interleukin-1beta  |2 NLM 
650 7 |a Lipopolysaccharides  |2 NLM 
650 7 |a Recombinant Fusion Proteins  |2 NLM 
650 7 |a Tumor Necrosis Factor-alpha  |2 NLM 
650 7 |a Interleukin-10  |2 NLM 
650 7 |a 130068-27-8  |2 NLM 
650 7 |a Peroxidase  |2 NLM 
650 7 |a EC 1.11.1.7  |2 NLM 
700 1 |a Wang, Bao-en  |e verfasserin  |4 aut 
700 1 |a Zheng, Xin-xiao  |e verfasserin  |4 aut 
700 1 |a Li, Min  |e verfasserin  |4 aut 
700 1 |a Mayer, Konstantin  |e verfasserin  |4 aut 
700 1 |a Zhang, Shu-wen  |e verfasserin  |4 aut 
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