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The Rapid Evolution of Chronic Inflammation to Tolerance / Immune Suppression: Mapping Bidirectional Checkpoints

ABSTRACT: The Rapid Evolution of Chronic Inflammation to Tolerance / Immune Suppression: Mapping Bidirectional Checkpoints

PROVIDER: PRJNA1099701 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28646782_1.fastq.gz	Fastqsanger.gz
	SRR28646782_2.fastq.gz	Fastqsanger.gz
	SRR28646783_1.fastq.gz	Fastqsanger.gz
	SRR28646783_2.fastq.gz	Fastqsanger.gz
	SRR28646784_1.fastq.gz	Fastqsanger.gz

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The Rapid Evolution of Chronic Inflammation to Tolerance / Immune Suppression: Mapping Bidirectional Checkpoints

Project description:Currently, there is truly a universal lack of knowledge as to exactly how chronic inflammation leads to the initiation of cancer. Likewise, there exists an equal deficiency in knowledge to define the phenomenon of immune “ tolerance”. Tolerance is, however, generally described as the diminished biological response to repeated or sustained antigen exposure associated with limitation to efficacy of toll-like receptor (TLR) synthetic lipid A lipoglycans, or microbial antigen molecular pattern (MAMP) based tumor immune therapies. The current work was designed to gain greater understanding into these questions, by employing a model of sustained antigenic TLR4 activation with gram-negative cell wall (LPS) for up to 11 days in macrophages under highly controlled conditions.

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MiR-221/222 suppression induced by activation of the cAMP/PKA/CREB1 pathway is required for cAMP-induced bidirectional differentiation of glioma cells [miRNA]

Project description:Factors that increase cAMP levels can induce lineage-specific differentiation of glioma cells into astrocyte-like cells. However, the differentiation pattern and underlying mechanisms remain unclear. Here, we find that cAMP/PKA/CREB1-induced miR-221/222 suppression contributes to the neuron-like differentiation of gliomas. cAMP agonists selectively induced neuron- and astrocyte-like but not oligodendrocyte-like differentiation of C6 glioma cells. PKA inhibitors and CREB1 knockout blocked neuron-like differentiation of glioma cells. cAMP inhibited miR-221/222 in a PKA/CREB1 dependent manner. Importantly, both in vitro and in vivo assays demonstrated that transcriptional suppression of miR-221/222 is required for neuronal differentiation of glioma cells. Our findings suggest that increasing cAMP levels can induce bidirectional differentiation of glioma cells. Furthermore, the miR-221/222 cluster acts as an epigenetic brake during glioma differentiation. Factors that increase cAMP levels can induce lineage-specific differentiation of glioma cells into astrocyte-like cells. However, the differentiation pattern and underlying mechanisms remain unclear. Here, we find that cAMP/PKA/CREB1-induced miR-221/222 suppression contributes to the neuron-like differentiation of gliomas. cAMP agonists selectively induced neuron- and astrocyte-like but not oligodendrocyte-like differentiation of C6 glioma cells. PKA inhibitors and CREB1 knockout blocked neuron-like differentiation of glioma cells. cAMP inhibited miR-221/222 in a PKA/CREB1 dependent manner. Importantly, both in vitro and in vivo assays demonstrated that transcriptional suppression of miR-221/222 is required for neuronal differentiation of glioma cells. Our findings suggest that increasing cAMP levels can induce bidirectional differentiation of glioma cells. Furthermore, the miR-221/222 cluster acts as an epigenetic brake during glioma differentiation.

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Project description:IL-10 limits the magnitude of inflammatory gene expression following microbial stimuli and is essential to prevent inflammatory disease, however, the molecular basis for IL-10 mediated inhibition remains elusive. Using a genome-wide approach we demonstrate that inhibition of transcription is the primary mechanism for IL-10-mediated suppression in LPS-stimulated macrophages, and that inhibited genes can be divided into two clusters. Genes in the first cluster are inhibited only if IL-10 is included early in the course of LPS stimulation and is strongly enriched for interferon-inducible genes. Genes in the second cluster can be rapidly suppressed by IL-10 even after transcription is initiated, and this is associated with suppression of LPS-induced enhancer activation. Interestingly, the ability of IL-10 to rapidly suppress active transcription exhibits a delay following LPS stimulation. Thus, a key pathway for IL-10 mediated suppression involves rapid inhibition of enhancer function during the secondary phase of the response to LPS.

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