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M6A RNA methylation mediates NOD1/NF-kB signaling activation in the liver of piglets challenged with lipopolysaccharide

ABSTRACT: m6A RNA methylation mediates NOD1/NF-kB signaling activation in the liver of piglets challenged with lipopolysaccharide

PROVIDER: PRJNA862730 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20665080_1.fastq.gz	Fastqsanger.gz
	SRR20665080_2.fastq.gz	Fastqsanger.gz
	SRR20665081_1.fastq.gz	Fastqsanger.gz
	SRR20665081_2.fastq.gz	Fastqsanger.gz
	SRR20665082_1.fastq.gz	Fastqsanger.gz

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m6A RNA methylation mediates NOD1/NF-kB signaling activation in the liver of piglets challenged with lipopolysaccharide

Project description:N6-methyladenosine (m6A) is the most abundant internal modification that widely participates in various immune and inflammatory responses, however, its regulatory mechanisms in the inflam-mation of liver induced by lipopolysaccharide in piglets remain largely unknown. In the present study, MeRIP-seq showed that 1166 and 1344 transcripts contained m6A methylation in control and LPS groups, respectively. The m6A methylation sites of these transcripts mainly distributes in the 5’ un-translated region (5’UTR), the coding sequence (CDS), and the 3’ untranslated region (3’UTR). In-terestingly, these genes were mostly enriched in the NF-κB signaling pathway, and LPS treatment significantly changed the m6A modification among NOD1, RIPK2, NFKBIA, NFKBIB and TNFAIP3 mRNAs.In conclusion, LPS activated the NOD1/NF-κB pathway at post-transcriptional regulation through changing m6A RNA methylation, and then promoted the overproduction of proinflammatory cytokines, ultimately resulting in liver inflammation and damage.

2022-10-06 | GSE209858 | GEO

M<sup>6</sup>A RNA Methylation Mediates NOD1/NF-kB Signaling Activation in the Liver of Piglets Challenged with Lipopolysaccharide.

Project description:N6-methyladenosine (m6A) is the most abundant internal modification that widely participates in various immune and inflammatory responses; however, its regulatory mechanisms in the inflammation of liver induced by lipopolysaccharide in piglets remain largely unknown. In the present study, piglets were intraperitoneally injected with 80 μg/kg LPS or an equal dose of sterile saline. Results indicated that LPS administration increased activities of serum alanine aminotransferase (ALT), induced M1 macrophage polarization and promoted secretion of inflammatory cytokines, and finally led to hepatic lesions in piglets. The NOD1/NF-κB signaling pathway was activated in the livers of the LPS group. Moreover, the total m6A level was significantly elevated after LPS treatment. MeRIP-seq showed that 1166 and 1344 transcripts contained m6A methylation in control and LPS groups, respectively. The m6A methylation sites of these transcripts mainly distributes in the 5' untranslated region (5'UTR), the coding sequence (CDS), and the 3' untranslated region (3'UTR). Interestingly, these genes were mostly enriched in the NF-κB signaling pathway, and LPS treatment significantly changed the m6A modification in NOD1, RIPK2, NFKBIA, NFKBIB, and TNFAIP3 mRNAs. In addition, knockdown of METTL3 or overexpression of FTO both changed gene levels in the NOD1/NF-κB pathway, suggesting that activation of this pathway was regulated by m6A RNA methylation. Moreover, the alteration of m6A RNA methylation profile may be associated with the increase of reactive oxygen species (ROS), HIF-1α, and MAT2A. In conclusion, LPS activated the NOD1/NF-κB pathway at post-transcriptional regulation through changing m6A RNA methylation, and then promoted the overproduction of proinflammatory cytokines, ultimately resulting in liver inflammation and damage.

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Nod1-dependent NF-kB activation initiates hematopoietic stem cell specification in response to small Rho GTPases

Project description:The possibility of specifying functional hematopoietic stem and progenitor cells (HSPCs) from human pluripotent stem cells (hPSCs) would overcome current limitations related to HSPC transplantation. However, generating hPSC-derived HSPCs has been elusive, necessitating a better understanding of the native developmental mechanisms that trigger HSPC specification. Here, we revealed in vivo an intrinsic inflammatory mechanism triggered by Nod1 that drives early hemogenic endothelium (HE) patterning to specify HSPCs. Our genetic and chemical experiments showed that HSPCs failed to specify in the absence of Nod1 and its downstream kinase Ripk2. Rescue experiments demonstrated that Nod1 and Ripk2 acted through NF-kB, and that small Rho GTPases are at the apex of this mechanism. Manipulation of NOD1 in a human system of hPSCs differentiation towards the definitive hematopoietic lineage indicated functional conservation. This work establishes the RAC1-NOD1-RIPK2-NFkB axis as the earliest inflammatory inductor that intrinsically primes the HE for proper HSPC specification. Manipulation of this pathway could help derive a competent HE amenable to specify functional patient specific HSPCs for the treatment of blood disorders. Keywords: NOD1, RIPK2, NF-kB, RAC1, Rho GTPases, Hematopoietic Stem and Progenitor Cell Specification, Hemogenic Endothelium.

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Project description:The change in the plasma proteome in chicken (Gallus gallus) challenged with lipopolysaccharide (endotoxin) derived from E. coli was determined by relative quantitation using a TMT label-based approach. This study provides insights into different factors contributing to innate immune response to experimental infection during 72 hours with special emphasis on acute phase proteins (APPs). Apart from APPs, several pathways endopeptidase activation and vasoconstriction were found to be significant.

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2017-09-03 | GSE101318 | GEO

Switching of the Relative Dominance Between Feedback Mechanisms in Lipopolysaccharide-Induced NF-kB Signaling

Project description:The bacterial product lipopolysaccharide (LPS) stimulates nuclear factor kB (NF-kB) signaling, which results in the production of proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha), as part of the immune response. NF-kB target genes also include those encoding proteins that inhibit NF-kB signaling through negative feedback loops. By simultaneously studying the dynamics of the nuclear translocation of the NF-kB subunit RelA and the activity of a Tnf-driven reporter in a mouse macrophage cell line, Sung et al. found that the gene encoding RelA was also a target of NF-kB. Synthesis of RelA occurred only at higher concentrations of LPS and constituted a positive feedback loop that dominated over existing negative feedback mechanisms. Genes expressed in response to a high concentration of LPS were enriched for those involved in innate immune responses. Together, these data suggest that the RelA-dependent positive feedback loop enables macrophages to mount an effective immune only above a critical concentration of LPS.

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Switching of the Relative Dominance Between Feedback Mechanisms in Lipopolysaccharide-Induced NF-kB Signaling

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Project description:Aberrant differentiation of progenitor cells in the hematopoietic system is known to severely impact host immune responsiveness. Here we demonstrate that NOD1, a cytosolic innate sensor of bacterial peptidoglycan, also functions in murine hematopoietic cells as a major regulator of both the generation and differentiation of lymphoid progenitors as well as peripheral T lymphocyte homeostasis. We further show that NOD1 mediates these functions by facilitating STAT5 signaling downstream of hematopoietic cytokines. In steady-state, loss of NOD1 resulted in a modest but significant decrease in numbers of mature T, B and NK cells. During systemic protozoan infection, this defect was markedly enhanced leading to host mortality. Lack of functional NOD1 also impaired T-cell-dependent anti-tumor immunity while preventing colitis. These findings reveal that in addition to its classical role as a bacterial ligand receptor, NOD1 plays an important function in regulating adaptive immunity through interaction with a major host cytokine signaling pathway.

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