Burn injury sensitizes rat Kupffer cells via mechanisms dependent on gut-derived endotoxin
Burn injury sensitizes rat Kupffer cells via mechanisms dependent on gut-derived endotoxin
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DOI：
10.1007/s00535-004-1468-9
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发表时间：
2004-12-01
影响因子：
6.3
通讯作者：
Sato, N
中科院分区：
文献类型：
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作者：
Enomoto, N;Takei, Y;Sato, N
背景热损伤后发生细菌移位，与肠屏障丧失相关。近年来，我们发现枯否细胞的致敏作用与肠源性内毒素有关，因此，本研究的目的是探讨烧伤后枯否细胞的致敏机制。方法.实验前24 h大鼠接受30%体表面积的全层蒸汽烧伤。检测血清丙氨酸氨基转移酶（ALT）以评估肝损伤，并检测门静脉血浆内毒素。在烧伤后24小时分离枯否细胞。使用荧光指示剂fura-2的显微荧光分光光度计测量枯否细胞中的细胞内钙（[Ca 2 +]（i）），并通过酶联免疫吸附试验（ELISA）测量肿瘤坏死因子（TNF）-α。结果烧伤治疗可增加脂多糖（LPS）诱导的死亡率。这种增加被库普弗细胞毒物氯化钆阻断。因此，枯否细胞参与了这一系统。LPS诱导的ALT升高被烧伤所上调。这种增加被抗生素预处理阻断。内毒素水平增加到几乎300 pg/ml（正常，
Background. Bacterial translocation occurs after thermal injury in association with intestinal barrier loss. Recently, we found that sensitization of Kupffer cells involved gut-derived endotoxin; therefore, the purpose of this work was to study the mechanisms of sensitization of Kupffer cells in burn injury. Methods. Rats received a 30% body surface area full-thickness steam burn 24 h before experiments. Serum alanine aminotransferase (ALT) was measured to assess liver damage, and plasma endotoxin in the portal vein were measured. Kupffer cells were isolated 24 h after the burn. Intracellular calcium ([Ca2+](i)) in Kupffer cells was measured using a microspectrofluorometer with the fluorescent indicator, fura-2, and tumor necrosis factor (TNF)-alpha was measured by enzyme-linked immunosorbent assay (ELISA). Results. Lipopolysaccharide (LPS)-induced mortality was increased by burn treatment. This increase was blocked by gadolinium chloride, a Kupffer-cell toxicant. Accordingly, Kupffer cells were involved in this system. The LPS-induced increase of ALT was upregulated by the burn injury. This increase was blocked by pretreatment with antibiotics. Endotoxin levels were increased to almost 300 pg/ml (normal,