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.