THE GUT - A CYTOKINE-GENERATING ORGAN IN SYSTEMIC INFLAMMATION

THE GUT - A CYTOKINE-GENERATING ORGAN IN SYSTEMIC INFLAMMATION
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DOI:
10.1097/00024382-199509000-00007
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发表时间:
1995-09-01
期刊:
影响因子:
3.1
通讯作者:
DEITCH, EA
DEITCH, EA
中科院分区:
医学2区
文献类型:
--
作者:
MAINOUS, MR;ERTEL, W;DEITCH, EA

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本研究的目的是检验肠道在致命或非致命炎症损伤后能够成为细胞因子生成器官的假设。成年雄性大鼠用盐水或非致死剂量 (0.1 mg/g) 或 LD(50) (0.5 mg/g) 剂量的酵母聚糖进行腹膜内攻击。在攻击后2、4、6、8或10小时获得肠系膜淋巴结、传出肠系膜淋巴、肝脏、脾脏和血液(门静脉和全身)。对器官、淋巴液和血液进行细菌易位(BT)检测;检测血液和淋巴液中的肿瘤坏死因子 (TNF) 和 IL-6。使用 0.1 mg/g 酵母聚糖后,BT 仅限于肠系膜淋巴结复合体; 0.5 mg/g 酵母聚糖促进 BT 进入血液、肠系膜淋巴和器官(与对照或 0.1 mg/g 酵母聚糖相比,p < 0.05)。门静脉菌血症的严重程度大于全身性菌血症 (p < .003)。血清 TNF 在酵母聚糖攻击后 2 小时达到峰值(p < .05 与对照相比),血清 IL-6 在 4-6 小时达到峰值(p < .05 与对照相比)。两种细胞因子的门静脉和全身生物活性相似,并且血清生物活性与酵母聚糖剂量不相关。仅用 0.5 mg/g 酵母聚糖攻击后 2 小时,肠系膜淋巴中的 TNF 生物活性增加(与对照或 0.1 mg/g 酵母聚糖相比,p < .05)。酵母聚糖攻击后 4 至 10 小时,肠系膜淋巴中的 IL-6 生物活性增加(与对照相比,p < 0.05),但与任一剂量的酵母聚糖相似。总之,即使在没有细菌门静脉或全身性传播的情况下,肠道也可能能够产生细胞因子来响应炎症刺激。细胞因子反应的强度与细菌易位的强度不相关。
The aim of this study was to test the hypothesis that the gut is capable of becoming a cytokine-generating organ following either a lethal or nonlethal inflammatory insult. Adult male rats were given an intraperitoneal challenge with saline, or with a nonlethal (.1 mg/g) or LD(50) (.5 mg/g) dose of zymosan. Mesenteric lymph nodes, efferent mesenteric lymph, liver, spleen, and blood (portal and systemic) were obtained at 2, 4, 6, 8, or 10 h post challenge. Organs, lymph, and blood were tested for bacterial translocation (BT); blood and lymph were assayed for tumor necrosis factor (TNF) and IL-6. After .1 mg/g zymosan, BT was limited to the mesenteric lymph node complex only; .5 mg/g zymosan promoted BT to blood, mesenteric lymph, and organs (p < .05 vs. control or .1 mg/g zymosan). The magnitude of portal bacteremia was greater than systemic bacteremia (p < .003). Serum TNF peaked at 2 h (p < .05 vs. control), and serum IL-6 peaked at 4-6 h (p < .05 vs. control) post zymosan challenge. Portal and systemic bioactivity was similar for either cytokine, and serum bioactivity did not correlate with zymosan dose. TNF bioactivity was increased in the mesenteric lymph at 2 h post challenge with .5 mg/g zymosan only (p < .05 vs. control or .1 mg/g zymosan). IL-6 bioactivity was increased in the mesenteric lymph at 4 through 10 h post zymosan challenge (p < .05 vs. control), but was similar with either dosage of zymosan. In conclusion, the gut may be capable of producing cytokines in response to an inflammatory stimulus, even in the absence of portal or systemic spread of bacteria. The magnitude of the cytokine response does not correlate with the magnitude of bacterial translocation.