Lactate production by Staphylococcus aureus biofilm inhibits HDAC11 to reprogramme the host immune response during persistent infection [ChIP-seq]. Lactate production by Staphylococcus aureus biofilm inhibits HDAC11 to reprogramme the host immune response during persistent infection [ChIP-seq]

Using ChIP-seq we show that total H3Ac within ± 10,000 bp of all genomic transcription start sites was decreased by approximately two-fold in MDSCs recovered from mice infected with a triple mutant, unable to make lactate, compared to WT S. aureus. Overall design: MDSCs for ChIP-seq were isolated from S. aureus-infected orthopedic implant-associated tissue at day 14 post-infection by FACS.

本研究通过染色质免疫共沉淀测序（ChIP-seq）证实，相较于野生型（WT）金黄色葡萄球菌（S. aureus），在感染了无法合成乳酸的三重突变株的小鼠体内分离得到的髓系来源抑制细胞（MDSCs）中，所有基因组转录起始位点（TSS）上下游±10000 bp范围内的总组蛋白H3乙酰化（H3Ac）水平降低了约两倍。实验整体设计：用于ChIP-seq的髓系来源抑制细胞（MDSCs）于感染后第14天，通过荧光激活细胞分选（FACS）从金黄色葡萄球菌感染的骨科植入物相关组织中分离获取。