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The response of the host microcirculation to bacterial sepsis: does the pathogen matter?

机译:宿主微循环对细菌性败血症的反应:病原体重要吗?

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摘要

Sepsis results from the interaction between a host and an invading pathogen. The microcirculatory dysfunction is now considered central in the development of the often deadly multiple organ dysfunction syndrome in septic shock patients. The microcirculatory flow shutdown and flow shunting leading to oxygen demand and supply mismatch at the cellular level and the local activation of inflammatory pathways resulting from the leukocyte–endothelium interactions are both features of the sepsis-induced microcirculatory dysfunction. Although the host response through the inflammatory and immunologic response appears to be critical, there are also evidences that Gram-positive and Gram-negative bacteria can exert different effects at the microcirculatory level. In this review we discuss available data on the potential bacterial-specific microcirculatory alterations observed during sepsis.
机译:败血症是由宿主和入侵病原体之间的相互作用引起的。现在认为在脓毒性休克患者中,通常致命的多器官功能障碍综合症的发展中,微循环功能障碍很重要。微循环流关闭和分流导致细胞水平上的氧气需求和供应失配,以及白细胞与内皮之间的相互作用导致的炎症途径的局部激活,都是败血症诱发的微循环功能障碍的特征。尽管通过炎症和免疫反应的宿主反应似乎至关重要,但也有证据表明革兰氏阳性和革兰氏阴性细菌可以在微循环水平上发挥不同的作用。在这篇综述中,我们讨论了败血症期间观察到的潜在细菌特异性微循环改变的可用数据。

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