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Oxidative Stress-initiated One-carbon Metabolism drives Interleukin-10-producing B Cells to Resolute Pneumonia (RNA-Seq)

ABSTRACT: Oxidative Stress-initiated One-carbon Metabolism drives Interleukin-10-producing B Cells to Resolute Pneumonia (RNA-Seq)

PROVIDER: PRJNA869765 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21070943.fastq.gz	Fastqsanger.gz
	SRR21070944.fastq.gz	Fastqsanger.gz
	SRR21070945.fastq.gz	Fastqsanger.gz
	SRR21070946.fastq.gz	Fastqsanger.gz
	SRR21070947.fastq.gz	Fastqsanger.gz

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Oxidative Stress-initiated One-carbon Metabolism drives Interleukin-10-producing B Cells to Resolute Pneumonia (ATAC-Seq)

Project description:Oxidative Stress-initiated One-carbon Metabolism drives Interleukin-10-producing B Cells to Resolute Pneumonia (ATAC-Seq)

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Oxidative Stress-initiated One-carbon Metabolism drives Interleukin-10-producing B Cells to Resolute Pneumonia (RNA-Seq)

Project description:Metabolic reprogramming for regulatory B cell generation in infectious diseases remains unknown. With a Pseudomonas aeruginosa-induced pneumonia model, we report IL-10-producing B cells (IL-10+B cells) are indispensable for spontaneous remission of the infection. The accumulation of cytosolic reactive oxygen species (ROS) is responsible for the IL-10 producing within B cells. Of note, ROS scavenging downregulated the one-carbon metabolism and the depletion of one-carbon metabolic methyl transfer enzyme serine hydroxymethyl transferase 1 (Shmt1) led to decreased IL-10+ B cells production both in vitro and in vivo. Mechanistically, one-carbon flux enhanced the availability of methyl groups, which altered histone H3 lysine 4 methylation at Il10 loci and led to massive IL-10 production in B cells. Therefore, the metabolic-associated drug ethacrynic acid (EA) was screened out and potentially restored infectious pneumonia accompanied by increased IL-10+ B cells. The results provide a new insight that ROS serve as modulators to resolute inflammation by reprogramming one-carbon metabolism in lung B cells.

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Oxidative Stress-initiated One-carbon Metabolism drives Interleukin-10-producing B Cells to Resolute Pneumonia (ATAC-Seq)

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Cell-specific Interleukin-15 and Interleukin-15 receptor subunit expression and regulation in pneumococcal pneumonia

Project description:IL-15 has critical impact on the homeostasis and activation of NK, NKT, gdT and CD8+T cells, and contributes to antimicrobial defenses particularly at mucosal sites. The respiratory tract also comprises a large mucosal surface and harbors significant amounts of lymphocytes, but the expression pattern of IL-15 in the lung and its role in local immune responses are largely unknown. We therefore analyzed the differential expression of IL-15 and the IL-15 receptor (IL-15R) complex in the lungs of mice, and demonstrated substantial constitutive expression in bronchial and alveolar epithelial cells, alveolar macrophages, and vascular smooth muscle cells, implicating contribution to pulmonary immune cell homeostasis already under normal conditions. The induction of pneumococcal pneumonia but not the infection with Chlamydophila pneumoniae evoked a significant up-regulation of IL-15 on alveolar macrophages and bronchial epithelial cells, with the latter presenting de-novo expression of IL-15 on their basolateral surface and additional up-regulation of IL-15Ra . Transcriptome analysis and semiquantitative PCR indicated at least partial transcriptional regulation. Finally, the increase of IL-15 was accompanied by enhanced expression of CD69, TNFa, IFNg and Bcl-2 by IL-15-dependent lymphocyte populations suggesting functional impact of IL-15 on the pulmonary immune response in pneumococcal pneumonia. Keywords: Streptococcus pneumoniae, pneumonia, IL-15

2006-03-01 | GSE3631 | GEO

Cell-specific Interleukin-15 and Interleukin-15 receptor subunit expression and regulation in pneumococcal pneumonia

Project description:IL-15 has critical impact on the homeostasis and activation of NK, NKT, gdT and CD8+T cells, and contributes to antimicrobial defenses particularly at mucosal sites. The respiratory tract also comprises a large mucosal surface and harbors significant amounts of lymphocytes, but the expression pattern of IL-15 in the lung and its role in local immune responses are largely unknown. We therefore analyzed the differential expression of IL-15 and the IL-15 receptor (IL-15R) complex in the lungs of mice, and demonstrated substantial constitutive expression in bronchial and alveolar epithelial cells, alveolar macrophages, and vascular smooth muscle cells, implicating contribution to pulmonary immune cell homeostasis already under normal conditions. The induction of pneumococcal pneumonia but not the infection with Chlamydophila pneumoniae evoked a significant up-regulation of IL-15 on alveolar macrophages and bronchial epithelial cells, with the latter presenting de-novo expression of IL-15 on their basolateral surface and additional up-regulation of IL-15Ra . Transcriptome analysis and semiquantitative PCR indicated at least partial transcriptional regulation. Finally, the increase of IL-15 was accompanied by enhanced expression of CD69, TNFa, IFNg and Bcl-2 by IL-15-dependent lymphocyte populations suggesting functional impact of IL-15 on the pulmonary immune response in pneumococcal pneumonia. Microarray experiments were done as two-color hybridizations. RNA labeling was performed with a Fluorescent Linear Amplification Kit (Agilent Technologies). In order to compensate dye specific effects, and to ensure statistically relevant data, a color swap was performed.

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Project description:Community-acquired pneumonia is a widespread disease with significant morbidity and mortality. Alveolar macrophages are tissue-resident lung cells that play a crucial role in innate immunity against bacteria causing pneumonia. We hypothesized that alveolar macrophages display adaptive characteristics after resolution of bacterial pneumonia. We studied mice one to six months after self-limiting lung infection due to Streptococcus pneumoniae, the most common cause of bacterial pneumonia. Among the myeloid cells recovered from the lung, only alveolar macrophages showed long-term modifications of their surface marker phenotype. The remodeling of alveolar macrophages was: (i) long-lasting (still observed 6 months post infection), (ii) regionally localized (only observed in the affected lobe after lobar pneumonia), and (iii) associated with a macrophage-dependent enhanced lung protection to another pneumococcal serotype. Metabolomic and transcriptomic profiling revealed that alveolar macrophages of mice which recovered from pneumonia had new baseline activities and altered responses to infection. Thus, the enhanced lung protection after mild and self-limiting respiratory infection includes a profound remodeling of alveolar macrophages that is long-lasting, compartmentalized, and manifest across surface receptors, metabolites, and both resting and stimulated transcriptomes. We used microarrays to detail the global program of gene expression for mouse alveolar macrophages sorted from lungs that were naïve or infected more than a month previously, at rest and during an acute (4-hour) infection.

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Altered gene expression in plasma of patients with pneumonia-induced sepsis compared to pneumonia without sepsis and healthy people

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Interleukin-36y-producing macrophages drive IL-17-mediated fibrosis.

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