Pulmonary Division and Groupe de Physiopathologie Respiratoire, Université de Sherbrooke, Sherbrooke, Quebec, Canada.
Shock. 2010 Apr;33(4):344-52. doi: 10.1097/SHK.0b013e3181c0f068.
Sepsis is exceedingly burdensome for hospital intensive care unit caregivers, and its incidence, as well as sepsis-related deaths, is increasing steadily. Sepsis is characterized by a robust increase in NO production throughout the organism that is driven by iNOS. Moreover, NO is an important factor in the development of septic shock and is synthesized by NOS, an enzyme expressed by a variety of cells, including vascular endothelium, macrophages, and neutrophils. However, the effects of NO on leukocyte functions, and the underlying mechanisms, are relatively unknown. Thus, the present review focuses on the effects of NO and its derivatives on cells of the immune system. Experimental evidences discussed herein show that NO induces posttranslational modifications of key proteins in targeted processes with the potential of deterring cellular physiology. Consequently, the manipulation of NO distribution in septic patients, used in conjunction with conventional treatments aimed at restoring normal immune functions, may represent a valuable therapeutic strategy.
脓毒症给医院重症监护病房的护理人员带来了极大的负担，其发病率以及与脓毒症相关的死亡率正在稳步上升。脓毒症的特征是整个机体中一氧化氮（NO）的产生大量增加，这是由诱导型一氧化氮合酶（iNOS）驱动的。此外，NO 是脓毒性休克发展的一个重要因素，由多种细胞表达的酶——一氧化氮合酶（NOS）合成，这些细胞包括血管内皮细胞、巨噬细胞和中性粒细胞。然而，NO 对白细胞功能的影响及其潜在机制尚不清楚。因此，本综述重点关注了 NO 及其衍生物对免疫系统细胞的影响。本文讨论的实验证据表明，NO 诱导靶向过程中关键蛋白的翻译后修饰，有可能抑制细胞生理学。因此，在脓毒症患者中操纵 NO 的分布，结合旨在恢复正常免疫功能的常规治疗，可能代表一种有价值的治疗策略。
