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犬弓首蛔虫抗原刺激大鼠肺泡巨噬细胞产生一氧化氮和前列腺素E2。

Toxocara canis antigens stimulate the production of nitric oxide and prostaglandin E2 by rat alveolar macrophages.

作者信息

Espinoza Elsa, Muro Antonio, Martín Manuel-Mario Sánchez, Casanueva Patricia, Pérez-Arellano José Luis

机构信息

Laboratorio de Parasitología. Facultad de Farmacia, Universidad de Salamanca, Spain.

出版信息

Parasite Immunol. 2002 Jun;24(6):311-9. doi: 10.1046/j.1365-3024.2002.00468.x.

DOI:10.1046/j.1365-3024.2002.00468.x
PMID:12102716
Abstract

The effect of four Toxocara canis antigens on nitric oxide (NO) and prostaglandin E2 (PGE2) synthesis was studied in vitro using rat alveolar macrophages. Somatic and excretory/secretory T. canis antigens prepared from adult worms and LII larvae were incubated with rat alveolar macrophages obtained by bronchoalveolar lavage at concentrations of 0.1-50 microg/ml. Both excretory/secretory adult antigen (ESA) and somatic LII antigen (SLII) stimulate the release of nitrites by alveolar macrophages. This effect was specific (inhibited by L-NAME and L-canavanine) and dose-dependent; 30 microg and 10 microg being the most effective concentrations of ESA and SLII, respectively. Western blot and reverse transcriptase-polymerase chain reaction analyses revealed that ESA antigen stimulates the production of NO at transcriptional level. T. canis ESA also stimulated macrophages to produce PGE2 at transcriptional level. The addition of L-canavanine decreased the release of PGE2 significantly, which suggests that NO mediates the production of this prostaglandin. These results indicate that T. canis can stimulate the release of vasodilatory mediators by macrophages of the host.

摘要

利用大鼠肺泡巨噬细胞在体外研究了四种犬弓首蛔虫抗原对一氧化氮(NO)和前列腺素E2(PGE2)合成的影响。从成虫和LII期幼虫制备的犬弓首蛔虫体抗原和排泄/分泌抗原,与通过支气管肺泡灌洗获得的大鼠肺泡巨噬细胞以0.1 - 50微克/毫升的浓度孵育。排泄/分泌成虫抗原(ESA)和体LII抗原(SLII)均刺激肺泡巨噬细胞释放亚硝酸盐。这种效应具有特异性(被L - 精氨酸甲酯和L - 刀豆氨酸抑制)且呈剂量依赖性;ESA和SLII最有效的浓度分别为30微克和10微克。蛋白质免疫印迹和逆转录聚合酶链反应分析显示,ESA抗原在转录水平刺激NO的产生。犬弓首蛔虫ESA还在转录水平刺激巨噬细胞产生PGE2。添加L - 刀豆氨酸显著降低了PGE2的释放,这表明NO介导了这种前列腺素的产生。这些结果表明,犬弓首蛔虫可刺激宿主巨噬细胞释放血管舒张介质。

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