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作 者:杨策[1] 周琳琳[1] 严军[1] 王海燕[1] 周建云 刘庆[1] 程英[1] 崔莉[1] 蒋建新[1]
机构地区:[1]第三军医大学大坪医院野战外科研究所第四研究室,全军交通医学研究所创伤,烧伤与复合伤国家重点实验室,重庆400042
出 处:《第三军医大学学报》2008年第21期1988-1993,共6页Journal of Third Military Medical University
基 金:国家重点基础研究发展计划(973计划)(2005CB522602);全军"十一五"科技攻关项目(06G080)~~
摘 要:目的下丘脑-垂体-肾上腺轴分泌的神经内分泌激素对天然免疫功能具有重要调控作用。本研究通过切除大鼠双侧肾上腺,观察冲击伤对大鼠主要天然免疫学指标的影响及其与模式识别受体表达的关系。方法Sprague-Dawley成年大鼠在肾上腺切除7d后遭受中度冲击伤,观察外周血白细胞数目,腹腔巨噬细胞吞噬大肠杆菌功能、肝脏、肺脏和肠系膜淋巴结细菌移位以及肺组织肿瘤坏死因子-α(TNF-α)的变化,进而检测肺组织SR-A、CD14、TLR4mRNA的表达。结果肾上腺切除抑制冲击伤后外周血白细胞减少,腹腔巨噬细胞吞噬功能减弱,肝、肺、肠系膜淋巴结细菌移位以及肺组织TNF-α分泌在肾上腺切除后也进一步增强。肺组织SR-A、CD14、TLR4mRNA在肾上腺切除后减少,并伴有显著的炎症反应和组织损伤。结论肾上腺激素能增强创伤后机体的天然免疫反应,且与SR-A、CD14、TLR4介导密切有关。Objective The regulation of neuroendocrine hormones on the innate immune responses remains controversial. This report investigated whether the adrenal-derived hormones directly enhanced the innate immune responses and alternation of main pattern recognition receptors in adrenalectomized rats following blast injury. Methods Bilateral adrenalectomy was performed on Sprague-Dawley adult rats, who inflicted with mild blast wave injury in 7 d later. Peripheral blood leukocyte counting, macrophage phagocytosis, bacterial translocation (BT) in lungs, livers and mesenteric lymph nodes (MLN) were measured and analyzed, and TNF-α level in the lung tissue was detected. The mRNA expressions of scavenger receptor-A (SR-A), CD14 and Toll like receptor-4 (TLR-4) were assessed with RT-PCR. Results After blast injury, the number of peripheral leukocytes was decreased ( P 〈 0.05 ), and the phagocytosis of peritoneal macrophages was increased (P 〈0.05), which were both reversed by adrenalectomy (P 〈 0.05). The gut-derived BT, TNF-α secretion were elevated in adrenalectomized rats (P 〈 0.05 ). Furthermore, the mRNA levels of SR-A, CD14 and TLR-4 in lung tissues of adrenalectomized rats were all decreased significantly. Adrenalectomized rats showed enhancement of inflammatory responses and severe tissue injuries. Conclusion Our data strongly indicate that the adrenal hormones can enhance the innate immune responses to the blast wave injury, at least partially via SR-A, CD14 and TLR-4.
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