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Nuclear adenine activation of hnRNPA2B1 promotes IL-1 transcription in antibacterial innate immunity [ATAC-seq]

ABSTRACT: Nuclear adenine activation of hnRNPA2B1 promotes IL-1 transcription in antibacterial innate immunity [ATAC-seq]

PROVIDER: PRJNA1096984 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28576482_1.fastq.gz	Fastqsanger.gz
	SRR28576482_2.fastq.gz	Fastqsanger.gz
	SRR28576483_1.fastq.gz	Fastqsanger.gz
	SRR28576483_2.fastq.gz	Fastqsanger.gz
	SRR28576484_1.fastq.gz	Fastqsanger.gz

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Nuclear adenine activation of hnRNPA2B1 promotes IL-1 transcription in antibacterial innate immunity [ATAC-seq]

Project description:Deciphering the rapid expression and the underlying mechanisms of antibacterial effectors is critical to host defense against bacterial infection. Bacterial infection can reprogram cellular metabolism, however, the immunometabolism and its cross-talk with epigenetics in the regulation of antibacterial innate immunity remain to be fully understood. Here we report that nuclear hnRNPA2B1 is required to antibacterial innate response by promoting Il1b transcription. Myeloid-specific Hnrnpa2b1-deficient mice are susceptible to bacterial infection, resulting from IL-1β production insufficiency. The screenings identify the metabolite adenine in the nucleus to be able to bind and activate hnRNPA2B1. Adenine directly recruits hnRNPA2B1 to Il1b enhancers for increasing chromatin accessibility to promote Il1b transcription through NCL and FTO-mediated DNA 6mA demethylation of Il1b gene enhancers. Furthermore, bacterial infection elevates nuclear adenine levels, and in vivo administration of adenine protects mice from bacterial infection through hnRNPA2B1-IL1 circuit. Our findings provide an undiscovered paradigm of cross-regulation between epigenetic and metabolic pathways in antibacterial innate immunity, adding insight and proposing new approach to the treatment of bacterial infections.

2025-04-28 | GSE263373 | GEO

Nuclear adenine activation of hnRNPA2B1 promotes IL-1 transcription in antibacterial innate immunity [Cut&Tag-seq]

2025-04-28 | GSE263374 | GEO

Nuclear adenine activation of hnRNPA2B1 promotes IL-1 transcription in antibacterial innate immunity [Cut&Tag-seq]

Project description:Nuclear adenine activation of hnRNPA2B1 promotes IL-1 transcription in antibacterial innate immunity [Cut&Tag-seq]

| PRJNA1096986 | ENA

Nuclear HNRNPA2B1 HITS-CLIP and RNA-seq

Project description:To identify HNRNPA2B1 binding sites on endogenous nuclear RNAs, we performed HITS-CLIP for endogenous HNRNPA2B1 and RNA-seq to analyze the nuclear RNA under either METTL3 or HNRNPA2B1 depletion. Wild type MDA-MB-231 cells were subjected to the HITS-CLIP procedure on immunoprecipitated HNRNPA2B1 associated RNA obtained from the nuclear fraction (Licatalosi D, et al. 2008, Nature 456:464-U22). For RNA-seq, nuclear RNA was extracted from MDA-MB-231 or Hela cells knocked down for METTL3 or HNRNPA2B1.

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Itaconate uptake via SLC13A3 improves hepatic antibacterial innate immunity

Project description:Itaconate is an immunoregulatory metabolite produced by the mitochondrial enzyme immune-responsive gene 1 (IRG1) in inflammatory macrophages. We recently identified an important mechanism by which itaconate is released from inflammatory macrophages. However, it remains unknown whether extracellular itaconate is taken up by non-myeloid cells to exert immunoregulatory functions. Here, we used a custom-designed CRISPR screen to identify the dicarboxylate transporter solute carrier family 13 member 3 (SLC13A3) as an itaconate importer and to characterize the role of SLC13A3 in itaconate-improved hepatic antibacterial innate immunity. Functionally, liver-specific deletion of Slc13a3 impairs hepatic antibacterial innate immunity in vivo and in vitro. Mechanistically, itaconate uptake via SLC13A3 induces transcription factor EB (TFEB)-dependent lysosomal biogenesis and subsequently improves antibacterial innate immunity in murine hepatocytes. These findings identify SLC13A3 as a key itaconate importer in murine hepatocytes and will aid in the development of potent itaconate-based antibacterial therapeutics.

2024-07-08 | GSE230735 | GEO

Nuclear HNRNPA2B1 HITS-CLIP and RNA-seq

2015-06-20 | GSE70061 | GEO

Itaconate uptake via SLC13A3 improves hepatic antibacterial innate immunity

Project description:Itaconate uptake via SLC13A3 improves hepatic antibacterial innate immunity

| PRJNA962479 | ENA

IL-33 controls IL-22-dependent antibacterial defense by modulating the microbiota [shotgun sequencing]

Project description:IL-22 plays a critical role in defending against mucosal infections, but how IL-22 production is regulated is incompletely understood. Here, we show that mice lacking IL-33 or its receptor ST2 (IL-1RL1) were more resistant to Streptococcus pneumoniae lung infection than wild-type animals, and that single nucleotide polymorphisms in IL33 and IL1RL1 were associated with pneumococcal pneumonia in humans. The effect of IL-33 on S. pneumoniae infection was mediated by negative regulation of IL-22 production by innate lymphoid cells (ILCs), but independent of ILC2s as well as IL-4 and IL-13 signaling. Moreover, IL-33´s influence on antibacterial defense was dependent on housing conditions of the mice, and mediated by the modulatory effect of IL-33 on the intestinal microbiota. Collectively, we reveal that IL-33 controls IL-22-dependent antibacterial defense by modulating the microbiota. Our study thus provides insight into the bidirectional crosstalk between the innate immune system and the microbiota and how it shapes susceptibility to bacterial infection.

2024-03-19 | GSE236343 | GEO

IL-33 controls IL-22-dependent antibacterial defense by modulating the microbiota [scRNA-seq]

2024-03-19 | GSE236342 | GEO

IL-33 controls IL-22-dependent antibacterial defense by modulating the microbiota [bulk RNA-seq]

Project description:IL-22 plays a critical role in defending against mucosal infections, but how IL-22 production is regulated is incompletely understood. Here, we show that mice lacking IL-33 or its receptor ST2 (IL-1RL1) were more resistant to Streptococcus pneumoniae lung infection than wild-type animals, and that single nucleotide polymorphisms in IL33 and IL1RL1 were associated with pneumococcal pneumonia in humans. The effect of IL-33 on S. pneumoniae infection was mediated by negative regulation of IL-22 production by innate lymphoid cells (ILCs), but independent of ILC2s as well as IL-4 and IL-13 signaling. Moreover, IL-33´s influence on antibacterial defense was dependent on the housing conditions of the mice, and mediated by IL-33´s modulatory effect on the intestinal microbiota. Collectively, we reveal that IL-33 controls IL-22-dependent antibacterial defense by modulating the microbiota. Our study thus provides insight into the bidirectional crosstalk between the innate immune system and the microbiota and how it shapes susceptibility to bacterial infection.

2024-03-19 | GSE236341 | GEO

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