Recent years have witnessed an emergence of interest in understanding metabolic changes associated with immune responses, termed immunometabolism. As oxygen is central to all aerobic metabolism, hypoxia is now recognized to contribute fundamentally to inflammatory and immune responses. Studies from a number of groups have implicated a prominent role for oxygen metabolism and hypoxia in innate immunity of healthy tissue (physiologic hypoxia) and during active inflammation (inflammatory hypoxia). This inflammatory hypoxia emanates from a combination of recruited inflammatory cells (e.g., neutrophils, eosinophils, and monocytes), high rates of oxidative metabolism, and the activation of multiple oxygen-consuming enzymes during inflammation. These localized shifts toward hypoxia have identified a prominent role for the transcription factor hypoxia-inducible factor (HIF) in the regulation of innate immunity. Such studies have provided new and enlightening insight into our basic understanding of immune mechanisms, and extensions of these findings have identified potential therapeutic targets. In this review, we summarize recent literature around the topic of innate immunity and mucosal hypoxia with a focus on transcriptional responses mediated by HIF.

中文翻译：

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缺氧和先天免疫：跟上 HIFsters 的步伐。

近年来，人们对了解与免疫反应相关的代谢变化（称为免疫代谢）产生了兴趣。由于氧气是所有有氧代谢的核心，因此现在认为缺氧从根本上促进炎症和免疫反应。许多小组的研究表明，氧代谢和缺氧在健康组织的先天免疫（生理性缺氧）和活动性炎症（炎症性缺氧）过程中发挥着重要作用。这种炎症性缺氧是由募集的炎症细胞（例如中性粒细胞、嗜酸性粒细胞和单核细胞）、高氧化代谢率以及炎症过程中多种耗氧酶的激活共同引起的。这些向缺氧的局部转变已经确定了转录因子缺氧诱导因子（HIF）在先天免疫调节中的重要作用。此类研究为我们对免疫机制的基本理解提供了新的、具有启发性的见解，并且这些发现的扩展已经确定了潜在的治疗靶点。在这篇综述中，我们总结了围绕先天免疫和粘膜缺氧主题的最新文献，重点关注 HIF 介导的转录反应。