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

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

PROVIDER: PRJNA559093 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9916710.fastq.gz	Fastqsanger.gz
	SRR9916711.fastq.gz	Fastqsanger.gz
	SRR9916712.fastq.gz	Fastqsanger.gz
	SRR9916713.fastq.gz	Fastqsanger.gz
	SRR9916714.fastq.gz	Fastqsanger.gz

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Lactate production by Staphylococcus aureus biofilm inhibits HDAC11 to reprogramme the host immune response during persistent infection

Project description:Lactate production by Staphylococcus aureus biofilm inhibits HDAC11 to reprogramme the host immune response during persistent infection

| PRJNA559090 | ENA

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

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

| PRJNA559092 | ENA

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

Project description: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.

2020-06-17 | GSE135494 | GEO

Lactate production by Staphylococcus aureus biofilm inhibits HDAC11 to reprogramme the host immune response during persistent infection.

Project description:Staphylococcus aureus is a leading cause of biofilm-associated prosthetic joint infection (PJI), resulting in considerable disability and prolonged treatment. It is known that host leukocyte IL-10 production is required for S. aureus biofilm persistence in PJI. An S. aureus bursa aurealis Tn library consisting of 1,952 non-essential genes was screened for mutants that failed to induce IL-10 in myeloid-derived suppressor cells (MDSCs), which identified a critical role for bacterial lactic acid biosynthesis. We generated an S. aureus ddh/ldh1/ldh2 triple Tn mutant that cannot produce D- or L-lactate. Co-culture of MDSCs or macrophages with ddh/ldh1/ldh2 mutant biofilm produced substantially less IL-10 compared with wild-type S. aureus, which was also observed in a mouse model of PJI and led to reduced biofilm burden. Using MDSCs recovered from the mouse PJI model and in vitro leukocyte-biofilm co-cultures, we show that bacterial-derived lactate inhibits histone deacetylase 11, causing unchecked HDAC6 activity and increased histone 3 acetylation at the Il-10 promoter, resulting in enhanced Il-10 transcription in MDSCs and macrophages. Finally, we show that synovial fluid of patients with PJI contains elevated amounts of D-lactate and IL-10 compared with control subjects, and bacterial lactate increases IL-10 production by human monocyte-derived macrophages.

| S-EPMC7529909 | biostudies-literature

Lactate production by Staphylococcus aureus biofilm inhibits HDAC11 to reprogramme the host immune response during persistent infection

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-06-17 | GSE135496 | GEO

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

Project description:scRNA-seq of CD45+ leukocytes isolated from WT and triple mutant-infected mice identified several genes with concordant changes in H3Ac status and transcriptional expression.

2020-06-17 | GSE135495 | GEO

Loss of HDAC11 leads to reduced secretion of MCP-1 and less severe EAE

Project description:HDAC11 regulates IL-10 expression and overexpression of HDAC11 in antigen presenting cells (APCs) leads to a pro-inflammatory phenotype. Conversely, loss of HDAC11 leads to upregulation of IL-10 and immune tolerance. HDAC11 overexpression is also associated with inflammatory diseases including multiple sclerosis. Hence we wished to determine the inflammatory mediators regulated by HDAC11. We used microarray to determine gene expression profile of macrophages from WT and HDAC11 knockout mice. Thioglycollate induced-peritoneal macrophages obtained from WT and HDAC11 knockout mice were used for total RNA extraction to determine changes in gene expression levels in macrophages from WT and HDAC11 knockout mice.

2014-03-31 | E-GEOD-56366 | biostudies-arrayexpress

Loss of HDAC11 leads to reduced secretion of MCP-1 and less severe EAE

2014-03-31 | GSE56366 | GEO

Transcriptomic analysis of day 1 (D1) differentiating WT and HDAC11-deficient mouse myoblasts

Project description:To get insight into the transcriptomic changes caused by HDAC11 loss at early myogenic differentiation, we performed RNA sequencing (RNA-Seq) in 24 h differentiated primary myoblasts from WT and HDAC11-deficient mice. Satellite cell-derived primary myoblasts were obtained after FACS isolation of skeletal muscle cells by growing them at low confluence in proliferation medium. To induce myoblast differentiation, cells were plated at high confluence and changed to differentiation media. Gene Ontology (GO) analysis of the genes upregulated in HDAC11 KO differentiating myoblasts revealed a statistically significant enrichment of cell cycle-related processes while the downregulated genes in HDAC11 KO differentiating myoblasts were enriched in “muscle system process” and “muscle contraction” GO categories.

2020-07-10 | GSE147423 | GEO

Stimulating BMP4 signaling via HDAC11 inhibition suppresses malignancy in preclinical models of human neuroblastoma

Project description:Bone morphogenetic proteins (BMPs) trigger as cell-extrinsic signals the differentiation of neural crest progenitor cells to the sympathoadrenal cell lineage. Human neuroblastoma derives from aberrant neural crest progenitor cells. We here show that histone deacetylase 11 (HDAC11), the most recently identified family member with, as yet, largely unknown function, is recruited to the BMP4 gene promoter and represses its transcription in neuroblastoma. Both HDAC11 depletion and enzymatic inhibition revert the epigenetic silencing of BMP4, thereby blocking a critical oncogenic function of HDAC11. Activated BMP4 signaling through targeting of HDAC11 induces a transcriptional profile predictive of favorable prognosis for patients when expressed in the tumors, indicating that the HDAC11-BMP4 axis plays a critical role for neuroblastoma biology. Furthermore, pathway activation causes MYCN proto-oncogene repression on a molecular level and anti-proliferative effects in functional assays in neuroblastoma cell lines and primary sphere cultures as well as strongly inhibiting tumor formation and growth of subcutaneous neuroblastoma xenografts in mice. For high-risk neuroblastoma, with cure rates below 30% using current treatment strategies, our work suggests a novel targeted therapeutic approach that would reactivate the developmental pathway inducing normal differentiation of neural crest progenitor cells.

2014-12-31 | GSE20399 | GEO

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