Objective To investigate whether P12，a kind of lipopolysaccharide（LPS）-binding protein（LBP） inhibitory peptide，could suppress the binding of LPS to alveolar macrophages（AMs） in a mouse model of endotoxemia in vivo.Methods Forty mice were randomly divided into five groups，ie.a control group，an endotoxemia group，a low dose P12-treated group，a middle dose P12-treated group and a high dose P12-treated group.Mouse model of endotoxemia was established by LPS injection intraperitoneally in the endotoxemia group and P12-treated groups.P12 was instilled via the tail vein.The effects of P12 on the binding of LPS to AMs were determined by flow cytometric analysis and quantization by mean fluorescence intensity(MFI).The productions of tumor necrosis factor α(TNF-α) in serum of mice were measured by enzyme-linked immunosorbent assay(ELISA).Results MFI in AMs from low，middle and high dose P12-treated groups was 40.08%，30.76% and 24.45%，respectively，which was higher than that of the control group(4.61%)，but less than that of the endotoxemic mice(45.31%).The concentration of TNF-α in serum of low，media and high dose P12-treated mice was (112.69±19.78)pg/mL，(86.34±9.25) pg/mL，(70.48±8.48)pg/mL respectively，which was higher than that of the control group[(24.88±5.82)pg/mL]，but less than that of the endotoxemic mice[(180.17±39.14)pg/mL].Conclusion The results suggest that P12 inhibit the binding of LPS and AMs，thus reduce the proudction of TNF-α stimulated by LPS.
Citation：
WU Xueling,ZHAO Yunfeng,QIAN Guisheng,XU Debin,CHEN Weizhong. Effects of lipopolysaccharide-binding protein inhibitory peptide on the binding of lipopolysaccharide to alveolar macrophages in a mouse model of endotoxemia. Chinese Journal of Respiratory and Critical Care Medicine, 2008, 08(3): 195-198. doi:
Copy
Copyright © the editorial department of Chinese Journal of Respiratory and Critical Care Medicine of West China Medical Publisher. All rights reserved
| 1. |
王兴鹏，吴丽颖，吴恺，等.脂多糖结合蛋白在实验性急性坏死型胰腺炎发生中的作用.中华医学杂志，2003，83：1619-1623.
|
| 2. |
Dentener MA，Vreugdenhil AC，Hoet PH，et al.Production of the acute-phase protein lipopolysaccharide-binding protein by respiratory type II epithelial cells：implications for local defense to bacterial endotoxins.Am J Respir Cell Mol Biol，2000，23：146-153.
|
| 3. |
Le Roy D，Di Padova F，Tees R，et al.Monoclonal antibodies to murine lipopolysaccharide (LPS)-binding protein (LBP) protect mice from lethal endotoxemia by blocking either the binding of LPS to LBP or the presentation of LPS/LBP complexes to CD14.J Immunol，1999，162：7454-7460.
|
| 4. |
徐德斌，钱桂生，侯一峰，等.脂多糖结合蛋白功能位点分析.解放军医学杂志，2004，29：85.
|
| 5. |
徐德斌，钱桂生，侯一峰，等.噬菌体展示短肽模拟脂多糖结合蛋白抗炎功能位点的研究.第三军医大学学报，2004，26：573-575.
|
| 6. |
Wu XL，Qian GS.Effect of LBP inhibitory peptide on U937 cells exposed to LPS.Respirology，2004，9（suppl）：A164.
|
| 7. |
吴学玲，钱桂生，徐德斌，等.肺损伤机制研究：脂多糖结合蛋白抑制肽对脂多糖诱导的人单核细胞株核转录因子κB活性的影响.中国临床康复，2005，9：89-91.
|
| 8. |
Knapp S，Wieland CW，van ’t Veer C，et al.Toll-like receptor 2 plays a role in the early inflammatory response to murine pneumococcal pneumonia but does not contribute to antibacterial defense.J Immunol，2004，172：3132-3138.
|
| 9. |
Polderman KH，Girbes AR.Drug intervention trials in sepsis：divergent results.Lancet，2004，363：1721-1723.
|
| 10. |
Chaby R.Strategies for the control of LPS-mediated pathophysiological disorders.Drug Discovery Today，1999，4：209-221.
|
| 11. |
吴学玲，钱桂生，赵云峰，等.脂多糖结合蛋白抑制肽抑制脂多糖与人单核巨噬细胞株的结合.中国病理生理杂志，2007，23：1392-1395.
|
| 12. |
Hamada M，Yamamoto S，Moriguchi S，et al.Phagocytosis of alveolar macrophages after conagenin injection to rats.J Antibiot，2001，54：349-353.
|
| 13. |
Le Roy D，Di Padova F，Adachi Y，et al.Critical role of lipopolysaccharide-binding protein and CD14 in immune responses against gram-negative bacteria.J Immunol，2001；167：2759-2765.
|
| 14. |
吴学玲，钱桂生，徐德斌，等.脂多糖结合蛋白抑制肽对内毒素诱导的U937细胞TLR4的影响.中国急救医学，2005，25：46-47.
|
| 15. |
吴学玲，钱桂生，徐德斌，等.脂多糖结合蛋白抑制肽对内毒素诱导的人单核巨噬细胞株表达CD14的影响.中国呼吸与危重监护杂志，2005，4：230-232.
|
| 16. |
Wu X，Qian G，Zhao Y，et al.LBP inhibitory peptide reduces endotoxin-induced macrophage activation and mortality.Inflamm Res，2005，54：451-457.
|
- 1. 王兴鹏，吴丽颖，吴恺，等.脂多糖结合蛋白在实验性急性坏死型胰腺炎发生中的作用.中华医学杂志，2003，83：1619-1623.
- 2. Dentener MA，Vreugdenhil AC，Hoet PH，et al.Production of the acute-phase protein lipopolysaccharide-binding protein by respiratory type II epithelial cells：implications for local defense to bacterial endotoxins.Am J Respir Cell Mol Biol，2000，23：146-153.
- 3. Le Roy D，Di Padova F，Tees R，et al.Monoclonal antibodies to murine lipopolysaccharide (LPS)-binding protein (LBP) protect mice from lethal endotoxemia by blocking either the binding of LPS to LBP or the presentation of LPS/LBP complexes to CD14.J Immunol，1999，162：7454-7460.
- 4. 徐德斌，钱桂生，侯一峰，等.脂多糖结合蛋白功能位点分析.解放军医学杂志，2004，29：85.
- 5. 徐德斌，钱桂生，侯一峰，等.噬菌体展示短肽模拟脂多糖结合蛋白抗炎功能位点的研究.第三军医大学学报，2004，26：573-575.
- 6. Wu XL，Qian GS.Effect of LBP inhibitory peptide on U937 cells exposed to LPS.Respirology，2004，9（suppl）：A164.
- 7. 吴学玲，钱桂生，徐德斌，等.肺损伤机制研究：脂多糖结合蛋白抑制肽对脂多糖诱导的人单核细胞株核转录因子κB活性的影响.中国临床康复，2005，9：89-91.
- 8. Knapp S，Wieland CW，van ’t Veer C，et al.Toll-like receptor 2 plays a role in the early inflammatory response to murine pneumococcal pneumonia but does not contribute to antibacterial defense.J Immunol，2004，172：3132-3138.
- 9. Polderman KH，Girbes AR.Drug intervention trials in sepsis：divergent results.Lancet，2004，363：1721-1723.
- 10. Chaby R.Strategies for the control of LPS-mediated pathophysiological disorders.Drug Discovery Today，1999，4：209-221.
- 11. 吴学玲，钱桂生，赵云峰，等.脂多糖结合蛋白抑制肽抑制脂多糖与人单核巨噬细胞株的结合.中国病理生理杂志，2007，23：1392-1395.
- 12. Hamada M，Yamamoto S，Moriguchi S，et al.Phagocytosis of alveolar macrophages after conagenin injection to rats.J Antibiot，2001，54：349-353.
- 13. Le Roy D，Di Padova F，Adachi Y，et al.Critical role of lipopolysaccharide-binding protein and CD14 in immune responses against gram-negative bacteria.J Immunol，2001；167：2759-2765.
- 14. 吴学玲，钱桂生，徐德斌，等.脂多糖结合蛋白抑制肽对内毒素诱导的U937细胞TLR4的影响.中国急救医学，2005，25：46-47.
- 15. 吴学玲，钱桂生，徐德斌，等.脂多糖结合蛋白抑制肽对内毒素诱导的人单核巨噬细胞株表达CD14的影响.中国呼吸与危重监护杂志，2005，4：230-232.
- 16. Wu X，Qian G，Zhao Y，et al.LBP inhibitory peptide reduces endotoxin-induced macrophage activation and mortality.Inflamm Res，2005，54：451-457.
