Endotoxin induces bacterial translocation and increases xanthine oxidase activity.
Endotoxin induces bacterial translocation and increases xanthine oxidase activity.
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内毒素诱导细菌移位并增加黄嘌呤氧化酶活性。
DOI：
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发表时间：
1989
期刊：
影响因子：
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通讯作者：
Rodney D. Berg
中科院分区：
文献类型：
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作者：
Edwin A. Deitch;Mary Taylor;M. Grisham;Li Ma;W. Bridges;Rodney D. Berg
在此之前，我们已证明内毒素可诱导肠道细菌移位，抑制或灭活黄嘌呤氧化酶活性可减少内毒素诱导的细菌移位。因此，进行了内毒素诱导的细菌易位与肠粘膜结构、黄嘌呤脱氢酶和氧化酶活性变化之间的关系的实验。腹腔注射大肠杆菌0111：B4内毒素(0.1 mg)24小时后，取ICR小鼠空肠、回肠、盲肠、近端结肠、远端结肠和肝脏组织。测定这些样品中黄嘌呤脱氢酶和氧化酶的活性，并与肠道形态相关。在接受内毒素的小鼠中，70%的细菌从肠道转移到肠外器官，而对照组小鼠的器官是无菌的(p<0.01)。内毒素主要损伤回肠和盲肠粘膜，增加回肠和肝脏黄嘌呤脱氢酶和盲肠氧化酶活性(p<0.05)。这些结果提示黄嘌呤氧化物酶诱导的粘膜损伤在内毒素诱导的细菌移位中起作用。
Previously, we documented that endotoxin induces bacterial translocation from the gut and that inhibition or inactivation of xanthine oxidase activity reduces endotoxin-induced bacterial translocation. Consequently, experiments were performed to correlate endotoxin-induced bacterial translocation with changes in intestinal mucosal structure and xanthine dehydrogenase and oxidase activity. Segments of the jejunum, ileum, cecum, proximal colon, distal colon, and liver were harvested from ICR mice 24 hr after IP administration of E. coli 0111:B4 endotoxin (0.1 mg). Xanthine dehydrogenase and oxidase activities were measured in these samples and correlated with intestinal morphology. Bacteria translocated from the intestines to extraintestinal organs in 70% of the mice receiving endotoxin, while the organs of control mice were sterile (p less than 0.01). Endotoxin injured primarily the ileal and cecal mucosa and increased ileal and hepatic xanthine dehydrogenase and cecal oxidase activities (p less than 0.05). These results suggest that xanthine oxidase-induced mucosal damage plays a role in endotoxin-induced bacterial translocation.