Whole transcriptome profiling of neutrophils (Gr1+) flow-sorted from the BM of PU.1 WT and PU.1 KO mice
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ABSTRACT:
PROVIDER: PRJNA434707 | ENA |
REPOSITORIES: ENA
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Project description:Neutrophils are essential first line defense cells against invading pathogens, yet their inappropriate activation contributes to immunological diseases and can cause collateral tissue damage. However, if and how neutrophils cell-intrinsically titrate their inflammatory response remains unknown. Here, we conditionally deleted PU.1, a key myeloid transcription factor, from the neutrophils of mice undergoing fungal infection, and then performed comprehensive epigenomic profiling. We find that a major function of PU.1 is to restrain the neutrophils’ immune response by broadly suppressing genomic enhancer outputs via recruiting histone deacetylase activity, thereby limiting the immune-stimulatory AP1-transcription factor JUNB from entering chromatin. Thus, neutrophils rely on a direct PU.1 repressor function as rheostat of the inflammatory chromatin state, safeguarding their epigenome from undergoing uncontrolled activation prior to pathogenic stimulation. We performed whole transcriptome profiling of neutrophils (Gr1+) flow-sorted from the BM of PU.1 WT and PU.1 KO mice, and found nearly 1000 differentially expressed transcripts, 443 of which were decreased and 555 increased in PU.1-deleted neutrophils. Functional annotations of the differentially expressed transcripts revealed that differentiation-associated gene sets were not significantly changed in the neutrophils from PU.1∆Neu mice. In contrast, the top ranked gene ontology (GO) sets downregulated in PU.1∆Neu neutrophils represented immunological terms such as inflammatory response, NFκB activity and Toll-like receptor (TLR) signalling.
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Project description:Six-weeks old (C57Bl6, Cx3cr1gfp/+) mice were intraperitonealy infected with a low number (1.104) of L. monocytogenes (EGDe strain) in exponential growth phase (bacteria were grown in BHI at 108/ml, and diluted 10.000x in PBS immediately before injection). Group of three mice were euthanized, before infection. Peritoneal cells were recovered by peritoneal lavage. Cells from individual mice were stained with antibodies to CD11b (PECy7), Gr1 (APC), NK1.1, B220 and CD3 (PE), and F4/80 (biotin-conjugated followed by streptavidinpacific blue) for sorting. Gr1- monocytes were purified as NK1.1- CD3- B220- CD11b+ F4/80low Gr1-, gfphigh; Gr1+ monocytes were purified as NK1.1- CD3- B220- CD11b+ F4/80low Gr1+, gfpint; and polymorphonuclear cells were purified as NK1.1- CD3- B220- CD11b+ F4/80- Gr1high, gfp-. 1.103 cells from each mice, time point, and phenotype were purified by facs sorting according to their phenotype. Samples were kept at 4°C before and during the sort. Cells were directly sorted in the SuperAmp Lysis Buffer (Miltenyi Biotec, Bergisch Gladbach, Germany) using a FACS Aria cell-sorter (BD biosciences).
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Project description:We sought to identify genes that are differentially regulated in CD11b+Gr1+ cells after tumor challenging. Mice were challenged with LLC-RFP cells (5×10^6 cells, subcutaneous injection) for 9 days. Single cell suspensions were prepared from lungs of both tumor challenged and control wild type mice and stained with antibodies against CD11b and Gr1. Approximately 1×10^5 CD11b+GR1+ myeloid progenitor cells were sorted by FACS (Aria II, BD Bioscience). Total RNA was extracted from the sorted cells for microarray analysis. In this dataset, we include the expression data of CD11b+Gr1+ cells obtained from both control wild type and tumor challenged mice. These data were used to obtain 22 genes that are upregulated in response to tumor challenging. We analyzed 3 samples from control mice and 2 samples tumor challenged mice. The mean values of the groups were used in the analysis. Genes that were upregulated >2 fold were sorted out and generate the table in the Matrix datasheet.
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Project description:Neutrophils are essential first line defense cells against invading pathogens, yet their inappropriate activation contributes to immunological diseases and can cause collateral tissue damage. However, neutrophil-intrinsic mechanisms adjusting an appropriate inflammatory response are unknown. Herein, we conditionally deleted PU.1, a key myeloid transcription factor, from the neutrophils of mice undergoing fungal infection, and then performed comprehensive epigenomic profiling. We find that a major function of PU.1 is to restrain the neutrophils’ immune response by broadly suppressing genomic enhancer outputs via recruiting histone deacetylase activity, thereby limiting the immune-stimulatory AP1-transcription factor JUNB from entering chromatin. Thus, PU.1 acts as rheostat of the inflammatory chromatin state, safeguarding the neutrophil epigenome from undergoing uncontrolled activation prior to pathogenic stimulation.
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