Abdominal aortic aneurysm (AAA) is a degenerative inflammatory disease with unknown etiology. AAA is characterized by abdominal aortic dilatation more than 3 cm and is often asymptomatic, but the rupture of aneurysm can lead to death. Age, smoking and male sex are major predisposing factors of AAA. This study compares the effect of Helicobacter (H.) pylori and Lactobacillus (L.) acidophilus on the cytokine profile of PBMCs of 5 men with abdominal aortic aneurysm (AAA) and 5 men with normal/insignificant angiography, CT-Scan and ultrasonography results in the single-culture and in the co-culture with HUVECs. IL-2, IL-4, IL-5, IL-6, IL-9, IL-10, IL-13, IL-17A, IL-17 F, IL-21, IL-22, IFN-γ and TNF-α were measured in culture supernatants using a commercial fluorescent-labeled-bead assay. In general, CagA+ H. pylori-extract induced higher production of IFN-γ, IL-13 and IL-21 by PBMCs. Treatment of patients' PBMCs with CagA+H. pylori-extract induced Th2 cytokines while treatment of controls' PBMCs with CagA+H. pylori-extract increased Th1 cytokines. In the co-culture, however, patients' PBMCs produced Th1 cytokines irrespective of extract treatment, while controls' PBMCs produced Th2 cytokines and decreased IL-10. CagA+ H. pylori- as well as L. acidophilus-extract induced higher levels of IL-9 by controls' PBMCs in co-culture with HUVECs than patients (P = 0.05 and P = 0.01). The cytokine pattern of PBMCs induced by CagA+ H. pylori- and L. acidophilus-extracts in the co-culture with HUVECs shows differences in AAA patients and in comparison to controls. Decreased secretion of IL-9, IL-21 and IL-22 by PBMCs of patients treated with CagA+ H. pylori extract in co-culture, as opposed to non-AAA controls may indicate the active role ECs play in AAA. Simultaneous production of IL-10 and Th1 cytokines in patients and pronounced Th2 cytokines in controls in response to both bacteria may point to the inherent differences between patients and controls, which need further investigation.

中文翻译：

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幽门螺杆菌和嗜酸乳杆菌提取物在腹主动脉瘤患者PBMCs中诱导的不同细胞因子模式。

腹主动脉瘤（AAA）是一种病因不明的变性炎症性疾病。AAA的特征是腹主动脉扩张超过3厘米，通常无症状，但动脉瘤破裂可导致死亡。年龄，吸烟和男性是AAA的主要诱因。本研究比较了幽门螺杆菌和嗜酸乳杆菌对5例腹主动脉瘤（AAA）男性和5例血管造影，CT扫描和超声检查结果正常/微不足道的男性PBMC细胞因子谱的影响与HUVEC一起进行单一培养和共培养。IL-2，IL-4，IL-5，IL-6，IL-9，IL-10，IL-13，IL-17A，IL-17F，IL-21，IL-22，IFN-γ和TNF使用商业荧光标记珠测定法在培养上清液中测量-α。通常，CagA +H。幽门螺杆菌提取物诱导PBMC产生更高的IFN-γ，IL-13和IL-21。用CagA + H治疗患者的PBMC。幽门螺杆菌提取物诱导Th2细胞因子，同时用CagA + H处理对照组的PBMC。幽门螺杆菌提取物增加Th1细胞因子。然而，在共培养中，患者的PBMCs产生Th1细胞因子，而与提取物处理无关，而对照的PBMCs产生Th2细胞因子并降低IL-10。在与HUVECs共培养时，CagA +幽门螺杆菌和嗜酸乳杆菌提取物通过对照PBMC诱导的IL-9水平高于患者（P = 0.05和P = 0.01）。在与HUVEC的共培养中，由CagA +幽门螺杆菌和嗜酸乳杆菌提取物诱导的PBMC的细胞因子模式在AAA患者中和与对照组相比有差异。IL-9分泌减少，与非AAA对照相反，在共培养中用CagA +幽门螺杆菌提取物治疗的患者的PBMC引起的IL-21和IL-22可能表明EC在AAA中发挥了积极作用。患者同时产生IL-10和Th1细胞因子以及对照中两种细菌均产生明显的Th2细胞因子，这可能表明患者和对照之间存在固有差异，需要进一步研究。