Department of Medicine, School of Medicine and Public Health (SMPH), University of Wisconsin-Madison, Madison, WI 53705, USA.
Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Cells. 2022 Jul 15;11(14):2210. doi: 10.3390/cells11142210.
Respiratory syncytial virus (RSV), or human orthopneumovirus, is a negative-sense RNA virus that is the causative agent of severe lower respiratory tract infections in children and is associated with exacerbations of adult lung disease. The mechanisms how severe and/or repetitive virus infections cause declines in pulmonary capacity are not fully understood. We have recently discovered that viral replication triggers epithelial plasticity and metabolic reprogramming involving the hexosamine biosynthetic pathway (HBP). In this study, we examine the relationship between viral induced innate inflammation and the activation of hexosamine biosynthesis in small airway epithelial cells. We observe that RSV induces ~2-fold accumulation of intracellular UDP-GlcNAc, the end-product of the HBP and the obligate substrate of N glycosylation. Using two different silencing approaches, we observe that RSV replication activates the HBP pathway in a manner dependent on the RELA proto-oncogene (65 kDa subunit). To better understand the effect of RSV on the cellular N glycoproteome, and its RELA dependence, we conduct affinity enriched LC-MS profiling in wild-type and RELA-silenced cells. We find that RSV induces the accumulation of 171 N glycosylated peptides in a RELA-dependent manner; these proteins are functionally enriched in integrins and basal lamina formation. To elaborate this mechanism of HBP expression, we demonstrate that RSV infection coordinately induces the HBP pathway enzymes in a manner requiring RELA; these genes include Glutamine-Fructose-6-Phosphate Transaminase 1 (GFPT)-1/2, Glucosamine-Phosphate N-Acetyltransferase (GNPNAT)-1, phosphoglucomutase (PGM)-3 and UDP-N-Acetylglucosamine Pyrophosphorylase (UAP)-1. Using small-molecule inhibitor(s) of 8-oxoguanine DNA glycosylase1 (OGG1), we observe that OGG1 is also required for the expression of HBP pathway. In proximity ligation assays, RSV induces the formation of a nuclear and mitochondrial RELA∙OGG1 complex. In co-immunoprecipitaton (IP) experiments, we discover that RSV induces Ser 536-phosphorylated RELA to complex with OGG1. Chromatin IP experiments demonstrate a major role of OGG1 in supporting the recruitment of RELA and phosphorylated RNA Pol II to the HBP pathway genes. We conclude that the RELA∙OGG1 complex is an epigenetic regulator mediating metabolic reprogramming and N glycoprotein modifications of integrins in response to RSV. These findings have implications for viral-induced adaptive epithelial responses.
呼吸道合胞病毒(RSV),或人类偏肺病毒,是一种负义 RNA 病毒,是儿童严重下呼吸道感染的病原体,并与成人肺部疾病的恶化有关。严重和/或反复的病毒感染如何导致肺功能下降的机制尚不完全清楚。我们最近发现,病毒复制会引发上皮细胞的可塑性和代谢重编程,涉及己糖胺生物合成途径(HBP)。在这项研究中,我们研究了病毒诱导的先天炎症与小气道上皮细胞中己糖胺生物合成的激活之间的关系。我们观察到 RSV 诱导细胞内 UDP-GlcNAc 的积累增加约 2 倍,UDP-GlcNAc 是 HBP 的终产物,也是 N 糖基化的必需底物。使用两种不同的沉默方法,我们观察到 RSV 复制以依赖 RELA 原癌基因(65 kDa 亚基)的方式激活 HBP 途径。为了更好地理解 RSV 对细胞 N 糖蛋白组及其 RELA 依赖性的影响,我们在野生型和 RELA 沉默细胞中进行了亲和富集 LC-MS 分析。我们发现 RSV 以 RELA 依赖的方式诱导 171 种 N 糖基化肽的积累;这些蛋白质在整合素和基底膜形成中功能丰富。为了阐述 HBP 表达的这种机制,我们证明 RSV 感染以依赖 RELA 的方式协调诱导 HBP 途径酶;这些基因包括谷氨酰胺-果糖-6-磷酸氨基转移酶 1(GFPT)-1/2、葡萄糖胺-磷酸 N-乙酰基转移酶(GNPNAT)-1、磷酸葡萄糖变位酶(PGM)-3 和 UDP-N-乙酰葡萄糖胺焦磷酸化酶(UAP)-1。使用 8-氧鸟嘌呤 DNA 糖基化酶 1(OGG1)的小分子抑制剂,我们观察到 OGG1 对于 HBP 途径的表达也是必需的。在接近连接测定中,RSV 诱导 RELA·OGG1 复合物的核和线粒体形成。在共免疫沉淀(IP)实验中,我们发现 RSV 诱导 Ser536 磷酸化的 RELA 与 OGG1 复合。染色质免疫沉淀实验表明,OGG1 在支持 RELA 和磷酸化 RNA Pol II 募集到 HBP 途径基因方面起着主要作用。我们得出结论,RELA·OGG1 复合物是一种表观遗传调节剂,介导代谢重编程和 RSV 诱导的整合素 N 糖蛋白修饰。这些发现对病毒诱导的适应性上皮反应具有重要意义。