HEPATIC INFLAMMATION IN RATS WITH EXPERIMENTAL SMALL INTESTINAL BACTERIAL OVERGROWTH
HEPATIC INFLAMMATION IN RATS WITH EXPERIMENTAL SMALL INTESTINAL BACTERIAL OVERGROWTH
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DOI：
10.1016/0016-5085(90)90833-m
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发表时间：
1990-02-01
期刊：
影响因子：
29.4
通讯作者：
SCHWAB, JH
中科院分区：
文献类型：
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作者：
LICHTMAN, SN;SARTOR, RB;SCHWAB, JH
肝胆炎症和其他肠外表现伴随某些肠道疾病，可能是由于管腔细菌或其炎性细胞壁成分的增殖或增强的运输。使用空肠自填充盲袢来创建小肠细菌过度生长，我们比较了3种大鼠品系中肝脏炎症的生化和组织学证据，这些大鼠品系选择用于对细菌细胞壁聚合物的可变炎症反应。建立SFBL后4周和12周，刘易斯和Wistar大鼠分别出现体重减轻、肝肿大和肝脏炎症。刘易斯大鼠4周后血浆天冬氨酸转氨酶水平（578 . ±. 77 U/L）和Wistar大鼠12 wk（220 . 35 U/L）显著高于具有自排空盲袢的大鼠（112 . ±. 24 U/L，p < 0.001; 104 . ±. 22，p < 0.05）或假手术刘易斯（84 . ±. 24，p < 0.001）或Wistar（78 . ±. 10，p < 0.001）大鼠。使用组织学分级评分进行的随机比较显示，转氨酶值异常。刘易斯和Wistar大鼠与自填充盲环肝损伤与胆管增生，纤维化和急性和慢性门静脉周围和局灶性实质炎症。具有自排空盲袢的刘易斯和Wistar大鼠偶尔出现轻度组织学病变。刘易斯大鼠自填盲环4 wk死亡率为50%，其他组仅为15%。然而，具有自填充盲袢的布法罗大鼠没有出现体重减轻、肝肿大或肝损伤。所有品系的血液、腹膜和肝脏厌氧培养均为阴性。饮食限制的假手术Wistar大鼠，其体重与具有自填充盲袢的Wistar大鼠相似，没有出现组织学异常或转氨酶水平升高（76 . ±. 31 U/L）。这些结果表明，实验性小肠细菌过度生长会导致敏感大鼠品系出现明显的肝脏炎症，从而导致纤维化。热量缺乏和肝脏细菌入侵不是病因。我们认为，细菌细胞壁聚合物或其他细菌毒素从盲环引起肝病变的遗传易感主机。
Hepatobiliary inflammation and other extraintestinal manifestations accompany certain intestinal disorders, perhaps because of proliferation or enhanced transport of luminal bacteria or their phlogistic cell-wall components. Using jejunal self-filling blind loops to create small bowel bacterial overgrowth, we compared biochemical and histological evidence of hepatic inflammation in 3 rat strains chosen for their variable inflammatory responses to bacterial cell wall polymers. Lewis and Wistar rats developed weight loss, hepatomegaly, and hepatic inflammation 4 and 12 wk, respectively, after creation of SFBL. Plasma aspartate aminotransferase levels in Lewis rats 4 wk (578 .+-. 77 U/L) and Wistar rats 12 wk (220 .+-. 35 U/L) after-self filling blind loops were significantly greater than in rats with self-emptying blind loops (112 .+-. 24 U/L, p < 0.001; 104 .+-. 22, p < 0.05) or sham-operated Lewis (84 .+-. 24, p < 0.001) or Wistar (78 .+-. 10, p < 0.001) rats. Randomized comparison using a histology grading score showed abnormalities that paralleled aminotransferase values. Lewis and Wistar rats with self-filling blind loops had hepatic injury with bile duct proliferation, fibrosis and acute and chronic periportal and focal parenchymal inflammation. Lewis and Wistar rats with self-emptying blind loops developed occasional mild histologic lesions. 50% of Lewis rats with self-filling blind loops for 4 wk died compared with only 15% in other groups. However, Buffalo rats with self-filling blind loops developed no weight loss, hepatomegaly, or hepatic injury, Anaerobic cultures of blood, peritoneum and liver were negative in all strains. Diet-restricted, sham-operated Wistar rats with weights similar to the Wistar rats with self-filling blind loops did not develop histologic abnormalities or elevated aminotransferase levels (76 .+-. 31 U/L). These results show that experimental small bowel bacterial overgrowth causes significant hepatic inflammation leading to fibrosis in susceptible rat strains. Caloric deprivation and hepatic bacterial invasion are not etiologically responsible. We suggest that bacterial cell wall polymers or other bacterial toxins from the blind loop cause hepatic lesions in genetically susceptible hosts.