Bauer P, Russell J M, Granger D N
Department of Molecular and Cellular Physiology, Louisiana State University Medical Center, Shreveport, Louisiana 71130-3932, USA.
Am J Physiol. 1999 Feb;276(2):G479-84. doi: 10.1152/ajpgi.1999.276.2.G479.
Products of enteric bacteria, including endotoxin [lipopolysaccharide (LPS)], have been implicated in the acute inflammatory responses elicited by ischemia and reperfusion (I/R) of the small intestine. The objective of this study was to assess the contribution of LPS to the increased E-selectin expression observed in the intestinal vasculature after I/R. The dual radiolabeled monoclonal antibody technique was used in LPS-sensitive (C3HeB/FeJ) and LPS-insensitive (C3H/HeJ) mice that were exposed to either exogenous LPS or to gut I/R (45 min ischemia, 5 h reperfusion). LPS elicited a dose-dependent (0.5-50 microgram LPS/animal) increase in E-selectin expression (at 3 h) in LPS-sensitive mice, whereas LPS-insensitive mice were largely unresponsive. E-selectin expression was increased fivefold by I/R in the small bowel of both LPS-sensitive and -insensitive mice. These results indicate that, although exogenous LPS is capable of eliciting profound dose-dependent increases in E-selectin expression, endogenous LPS does not contribute significantly to I/R-induced expression of this endothelial cell adhesion molecule.
肠道细菌的产物，包括内毒素[脂多糖（LPS）]，与小肠缺血再灌注（I/R）引发的急性炎症反应有关。本研究的目的是评估LPS对I/R后在肠道血管中观察到的E-选择素表达增加的作用。双放射性标记单克隆抗体技术用于对LPS敏感（C3HeB/FeJ）和对LPS不敏感（C3H/HeJ）的小鼠，这些小鼠要么暴露于外源性LPS，要么经历肠道I/R（45分钟缺血，5小时再灌注）。LPS在LPS敏感小鼠中引起E-选择素表达（3小时时）呈剂量依赖性（0.5-50微克LPS/只动物）增加，而LPS不敏感小鼠基本无反应。在LPS敏感和不敏感小鼠的小肠中，I/R均使E-选择素表达增加了五倍。这些结果表明，虽然外源性LPS能够引起E-选择素表达显著的剂量依赖性增加，但内源性LPS对I/R诱导的这种内皮细胞粘附分子的表达没有显著作用。
