PDF(Pubmed)
Abstract：
BACKGROUND: Ticks are vectors of various pathogens, including tick-borne encephalitis virus causing TBE and bacteria such as Borrelia burgdorferi sensu lato and Anaplasma phagocytophilum causing e.g. viral-bacterial co-infections (TBE + LB/HGA), which pose diagnostic and therapeutic problems. Since these infections are usually accompanied by inflammation and oxidative stress causing metabolic modifications, including phospholipids, the aim of the study was to assess the level of polyunsaturated fatty acids and their metabolism (ROS- and enzyme-dependent) products in the blood plasma of patients with TBE and TBE + LB/HGA before and after pharmacotherapy.
METHODS: The total antioxidant status was determined using 2,20-azino-bis-3-ethylbenzothiazolin-6-sulfonic acid. The phospholipid and free fatty acids were analysed by gas chromatography. Lipid peroxidation was estimated by measuring small molecular weight reactive aldehyde, malondialdehyde and neuroprostanes. The reactive aldehyde was determined using gas chromatography coupled with mass spectrometry. The activity of enzymes was examined spectrophotometrically. An analysis of endocannabinoids and eicosanoids was performed using a Shimadzu UPLC system coupled with an electrospray ionization source to a Shimadzu 8060 Triple Quadrupole system. Receptor expression was measured using an enzyme-linked immunosorbent assay (ELISA).
RESULTS: The reduced antioxidant status as a result of infection was accompanied by a decrease in the level of phospholipid arachidonic acid (AA) and docosahexaenoic acid (DHA) in TBE, an increase in DHA in co-infection and in free DHA in TBE with an increase in the level of lipid peroxidation products. The enhanced activity of enzymes metabolizing phospholipids and free PUFAs increased the level of endocannabinoids and eicosanoids, while decreased 15-PGJ2 and PGE2 was accompanied by activation of granulocyte receptors before pharmacotherapy and only tending to normalize after treatment.
CONCLUSIONS: Since classical pharmacotherapy does not prevent disorders of phospholipid metabolism, the need to support treatment with antioxidants may be suggested.
METHODS: The total antioxidant status was determined using 2,20-azino-bis-3-ethylbenzothiazolin-6-sulfonic acid. The phospholipid and free fatty acids were analysed by gas chromatography. Lipid peroxidation was estimated by measuring small molecular weight reactive aldehyde, malondialdehyde and neuroprostanes. The reactive aldehyde was determined using gas chromatography coupled with mass spectrometry. The activity of enzymes was examined spectrophotometrically. An analysis of endocannabinoids and eicosanoids was performed using a Shimadzu UPLC system coupled with an electrospray ionization source to a Shimadzu 8060 Triple Quadrupole system. Receptor expression was measured using an enzyme-linked immunosorbent assay (ELISA).
RESULTS: The reduced antioxidant status as a result of infection was accompanied by a decrease in the level of phospholipid arachidonic acid (AA) and docosahexaenoic acid (DHA) in TBE, an increase in DHA in co-infection and in free DHA in TBE with an increase in the level of lipid peroxidation products. The enhanced activity of enzymes metabolizing phospholipids and free PUFAs increased the level of endocannabinoids and eicosanoids, while decreased 15-PGJ2 and PGE2 was accompanied by activation of granulocyte receptors before pharmacotherapy and only tending to normalize after treatment.
CONCLUSIONS: Since classical pharmacotherapy does not prevent disorders of phospholipid metabolism, the need to support treatment with antioxidants may be suggested.
摘要：
背景：蜱是各种病原体的载体，包括引起TBE的蜱传脑炎病毒和细菌，如伯氏疏螺旋体和吞噬菌体，如病毒-细菌共感染（TBE+LB/HGA），造成诊断和治疗问题。由于这些感染通常伴有炎症和氧化应激引起代谢改变，包括磷脂,本研究的目的是评估TBE和TBE+LB/HGA患者药物治疗前后血浆中多不饱和脂肪酸及其代谢产物(ROS和酶依赖性)的水平.
方法：使用2,20-氮杂-双-3-乙基苯并噻唑啉-6-磺酸测定总抗氧化剂状态。通过气相色谱法分析磷脂和游离脂肪酸。脂质过氧化通过测量小分子量反应性醛来估计，丙二醛和神经前列腺素。使用气相色谱与质谱联用测定反应性醛。用分光光度法检查酶的活性。使用ShimadzuUPLC系统与电喷雾电离源耦合到Shimadzu8060三重四极杆系统，对内源性大麻素和类二十烷酸进行了分析。使用酶联免疫吸附测定(ELISA)测量受体表达。
结果：由于感染而降低的抗氧化状态伴随着TBE中磷脂花生四烯酸（AA）和二十二碳六烯酸（DHA）水平的降低，随着脂质过氧化产物水平的增加，合并感染中DHA和TBE中游离DHA的增加。代谢磷脂和游离PUFA的酶的活性增强增加了内源性大麻素和二十烷酸的水平，而15-PGJ2和PGE2的降低在药物治疗前伴随着粒细胞受体的激活，并且仅在治疗后趋于正常化。
结论：由于经典药物治疗不能预防磷脂代谢紊乱，可能需要支持抗氧化剂治疗。
方法：使用2,20-氮杂-双-3-乙基苯并噻唑啉-6-磺酸测定总抗氧化剂状态。通过气相色谱法分析磷脂和游离脂肪酸。脂质过氧化通过测量小分子量反应性醛来估计，丙二醛和神经前列腺素。使用气相色谱与质谱联用测定反应性醛。用分光光度法检查酶的活性。使用ShimadzuUPLC系统与电喷雾电离源耦合到Shimadzu8060三重四极杆系统，对内源性大麻素和类二十烷酸进行了分析。使用酶联免疫吸附测定(ELISA)测量受体表达。
结果：由于感染而降低的抗氧化状态伴随着TBE中磷脂花生四烯酸（AA）和二十二碳六烯酸（DHA）水平的降低，随着脂质过氧化产物水平的增加，合并感染中DHA和TBE中游离DHA的增加。代谢磷脂和游离PUFA的酶的活性增强增加了内源性大麻素和二十烷酸的水平，而15-PGJ2和PGE2的降低在药物治疗前伴随着粒细胞受体的激活，并且仅在治疗后趋于正常化。
结论：由于经典药物治疗不能预防磷脂代谢紊乱，可能需要支持抗氧化剂治疗。
