Institute for Experimental Infection Research, Centre for Experimental and Clinical Infection Research, a joint venture between The Helmholtz-Centre for Infection Research, Hannover Medical School, TWINCORE, Feodor-Lynen-Str. 7, 30625, Hannover, Germany.
Department of Pathology, University of Veterinary Medicine Hannover, 30559, Foundation, Hannover, Germany.
J Neuroinflammation. 2024 Aug 17;21(1):203. doi: 10.1186/s12974-024-03197-2.
Microglia serve as a front-line defense against neuroinvasive viral infection, however, determination of their actual transcriptional profiles under conditions of health and disease is challenging. Here, we used various experimental approaches to delineate the transcriptional landscape of microglia during viral infection. Intriguingly, multiple activation genes were found to be artificially induced in sorted microglia and we demonstrated that shear stress encountered during cell sorting was one of the key inducers. Post-hoc analysis revealed that publicly available large-scale single-cell RNA sequencing datasets were significantly tainted by aberrant signatures that are associated with cell sorting. By exploiting the ribosomal tagging approach, we developed a strategy to enrich microglia-specific transcripts by comparing immunoprecipitated RNA with total RNA. Such enriched transcripts were instrumental in defining bona fide signatures of microglia under conditions of health and virus infection. These unified microglial signatures may serve as a benchmark to retrospectively assess ex vivo artefacts from available atlases. Leveraging the microglial translatome, we found enrichment of genes implicated in T-cell activation and cytokine production during the course of VSV infection. These data linked microglia with T-cell re-stimulation and further underscored that microglia are involved in shaping antiviral T-cell responses in the brain. Collectively, our study defines the transcriptional landscape of microglia under steady state and during viral encephalitis and highlights cellular interactions between microglia and T cells that contribute to the control of virus dissemination.
小胶质细胞作为抵御神经入侵性病毒感染的第一道防线,然而,确定它们在健康和疾病状态下的实际转录谱是具有挑战性的。在这里,我们使用了各种实验方法来描绘病毒感染中小胶质细胞的转录图谱。有趣的是,我们发现多个激活基因在分选的小胶质细胞中被人为诱导,并且我们证明细胞分选过程中遇到的切应力是其中的关键诱导因素之一。事后分析表明,公开的大规模单细胞 RNA 测序数据集受到与细胞分选相关的异常特征的显著污染。通过利用核糖体标记方法,我们开发了一种策略,通过比较免疫沉淀 RNA 与总 RNA 来富集小胶质细胞特异性转录本。这些富集的转录本对于定义健康和病毒感染条件下小胶质细胞的真实特征至关重要。这些统一的小胶质细胞特征可作为基准,用于回顾性评估现有图谱中体外的人为假象。利用小胶质细胞翻译组,我们发现,在 VSV 感染过程中,与 T 细胞激活和细胞因子产生相关的基因富集。这些数据将小胶质细胞与 T 细胞再刺激联系起来,并进一步强调小胶质细胞参与塑造大脑中的抗病毒 T 细胞反应。总的来说,我们的研究定义了稳态和病毒性脑炎中小胶质细胞的转录图谱,并强调了小胶质细胞与 T 细胞之间的细胞相互作用,有助于控制病毒的传播。