Helicobacter pylori infection selectively attenuates endothelial function in male mice via exosomes-mediated ROS production.
Helicobacter pylori infection selectively attenuates endothelial function in male mice via exosomes-mediated ROS production.
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DOI：
10.3389/fcimb.2023.1142387
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发表时间：
2023
影响因子：
5.7
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中科院分区：
文献类型：
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动脉粥样硬化存在显著的性别差异。过多的ROS形成可导致内皮功能障碍，而内皮功能障碍是动脉粥样硬化发生发展的关键。幽门螺杆菌(H.Pylori)感染可通过外切体介导的ROS形成来减弱内皮功能。我们已经证明，幽门螺杆菌感染选择性地增加男性动脉粥样硬化的风险，机制不明(S)。本研究旨在验证幽门螺杆菌感染通过外显子介导的ROS形成选择性损害雄性小鼠血管内皮细胞功能的假设。用CagA+H.Pylori感染年龄匹配的雄性和雌性C57BL/6小鼠，研究Hp感染诱导的内皮功能障碍的性别差异。幽门螺杆菌感染减弱了乙酰胆碱(ACh)诱导的内皮依赖性的主动脉松弛，但不改变硝酸甘油诱导的非内皮依赖性的松弛，与对照组相比，这种作用可被N-乙酰半胱氨酸逆转。用幽门螺杆菌感染的雄性(而不是雌性)小鼠的外切体处理培养的小鼠脑微血管内皮细胞，显著增加细胞内ROS的产生，并损害内皮功能，减少迁移、管状形成和增殖，这可以用N-乙酰半胱氨酸治疗来防止。幽门螺杆菌感染通过外切体介导的ROS形成选择性地损害雄性小鼠的内皮功能。
Substantial sex differences exist in atherosclerosis. Excessive reactive oxygen species (ROS) formation could lead to endothelial dysfunction which is critical to atherosclerosis development and progression. Helicobacter pylori (H. pylori) infection has been shown to attenuate endothelial function via exosomes-mediated ROS formation. We have demonstrated that H. pylori infection selectively increases atherosclerosis risk in males with unknown mechanism(s). The present study was to test the hypothesis that H. pylori infection impaired endothelial function selectively in male mice through exosome-mediated ROS formation. Age-matched male and female C57BL/6 mice were infected with CagA+ H. pylori to investigate sex differences in H. pylori infection-induced endothelial dysfunction. H. pylori infection attenuated acetylcholine (ACh)-induced endothelium-dependent aortic relaxation without changing nitroglycerine-induced endothelium-independent relaxation in male but not female mice, associated with increased ROS formation in aorta compared with controls, which could be reversed by N-acetylcysteine treatment. Treatment of cultured mouse brain microvascular endothelial cells with exosomes from H. pylori infected male, not female, mice significantly increased intracellular ROS production and impaired endothelial function with decreased migration, tube formation, and proliferation, which could be prevented with N-acetylcysteine treatment. H. pylori infection selectively impairs endothelial function in male mice due to exosome-mediated ROS formation.
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