Ghezzi Pietro
Brighton and Sussex Medical School, Brighton, Great Britain, BN1 9RY, UK.
Redox Biol. 2021 Aug;44:102001. doi: 10.1016/j.redox.2021.102001. Epub 2021 May 8.
It is thought that excessive production of reactive oxygen species (ROS) can be a causal component in many diseases, some of which have an inflammatory component. This led to an oversimplification whereby ROS are seen as inflammatory and antioxidants anti-inflammatory. This paper aims at reviewing some of the literature on thiols in host defense. The review will first summarize the mechanisms by which we survive infections by pathogens. Then we will consider how the redox field evolved from the concept of oxidative stress to that of redox regulation and how it intersects the field of innate immunity. A third section will analyze how an oversimplified oxidative stress theory of disease led to a hypothesis on the role of ROS and glutathione (GSH) in immunity, respectively as pro- and anti-inflammatory mediators. Finally, we will discuss some recent research and how to think out of the box of that oversimplification and link the role of thiols in redox regulation to the mechanisms by which we survive an infection outlined in the first section.
人们认为，活性氧（ROS）的过度产生可能是许多疾病的一个致病因素，其中一些疾病具有炎症成分。这导致了一种过度简化的观点，即ROS被视为具有炎症性，而抗氧化剂具有抗炎性。本文旨在综述一些关于宿主防御中硫醇的文献。该综述将首先总结我们在病原体感染中存活的机制。然后，我们将探讨氧化还原领域是如何从氧化应激概念发展到氧化还原调节概念的，以及它如何与固有免疫领域交叉。第三部分将分析疾病的过度简化的氧化应激理论如何分别导致了关于ROS和谷胱甘肽（GSH）在免疫中作为促炎和抗炎介质作用的假设。最后，我们将讨论一些最近的研究，以及如何突破这种过度简化的思维定式，将硫醇在氧化还原调节中的作用与第一部分所述的我们在感染中存活的机制联系起来。
