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Hydrogen gas inhibits the formation of neutrophil extracellular traps

ABSTRACT: Hydrogen gas inhibits the formation of neutrophil extracellular traps

PROVIDER: PRJNA741395 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14911005_1.fastq.gz	Fastqsanger.gz
	SRR14911005_2.fastq.gz	Fastqsanger.gz
	SRR14911006_1.fastq.gz	Fastqsanger.gz
	SRR14911006_2.fastq.gz	Fastqsanger.gz
	SRR14911007_1.fastq.gz	Fastqsanger.gz

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Hydrogen gas inhibits the formation of neutrophil extracellular traps

Project description:Neutrophil extracellular traps (NETs) contribute to inflammatory pathogenesis, especially in infectious and cardiovascular diseases. H2 gas acts as an antioxidant and has been clinically and experimentally proven to ameliorate inflammation. Therefore, we investigated whether H2 gas could inhibit NET formation associated with excessive neutrophil activation. Phorbol-12-myristate-13-acetate (PMA)-stimulated human neutrophils exposed to H2 exhibited reduced citrullination of histones, membrane disruption by chromatin complexes, and release of NET components over controls. Mechanistically, H2 suppressed the phosphorylation of Ser-139 residue in H2AX, a marker of DNA damage, thereby reducing the expression of CXC-chemokine receptor 4 (CXCR4) in PMA-stimulated neutrophils. Along with the upregulation of CXCR4, the intracellular content of myeloperoxidase (MPO) and the production of MPO-derived hypochlorous acid (HOCl) was increased; however, these effects were markedly suppressed in H2-exposed cultures. Thus, H2 neutralized HOCl produced by the oxidative burst, inhibited DNA damage, and subsequently inhibited NET formation. We further confirmed that inhalation of H2 inhibited the formation and release of NET components in the blood and bronchoalveolar lavage of a lipopolysaccharide-induced sepsis model in mice and aged minipigs. Therefore, H2 therapy has the potential to be a new therapeutic agent for inflammatory diseases involving NETs associated with excessive neutrophil activation.

2022-02-23 | GSE178883 | GEO

Specific post-translational histone mod. of neutrophil extracellular traps as immunogens & potential SLE Ab targets.

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How post-translational modification of nitrogenase is circumvented in Rhodopseudomonas palustris strains that produce hydrogen gas constitutively

Project description:Characterization of post-translational modification of nitrogenase in Rhodopseudomonas palustris strains that produce hydrogen gas constitutively.

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Hydrogen gas therapy attenuate inflammatory pathway signaling in septic mice

Project description:Molecular hydrogen (H2) has been used in several clinical cases. However, few studies have been reported on the use of hydrogen therapy for treatment of sepsis, and the anti-inflammatory mechanism of H2 remains majorly unknown. The aim of this study is to confirm the effects of H2 therapy for sepsis and reveal its therapeutic mechanism by performing RNA-seq in multiple organs in the septic mice. Nine-week-old C57BL/6 male mice underwent cecal ligation and puncture procedure (CLP) or sham procedure. Subsequently, the CLP model received an immediate +/- continuous inhalation of 7% H2. The H2 gas-treated groups were housed in the same cage, and they were put in a designated box that was able to maintain the concentration of H2 through constant H2 supply by a gas generator. Mice were observed for a week to assess their survival rates. Serum inflammatory cytokines were evaluated with ELISA at 24 h after the CLP procedure.

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Project description:Cerebral Cavernous Malformation (CCM) is a brain vascular disease with various neurological symptoms. In this study, we describe the inflammatory profile in CCM and show for the first time the formation of neutrophil extracellular traps (NETs) in rodents and humans with CCM. Through RNA-seq analysis of cerebellum endothelial cells from wild-type mice and mice with anendothelial cell-specific ablation of the Ccm3 gene (Ccm3iECKO), we show that endothelial cells from Ccm3iECKO mice have anincreased expression of inflammation-related genes.

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Project description:Neutrophil recruitment and activation are hallmarks of the prevalent inflammatory disease, periodontitis. However, the mechanisms by which neutrophils contribute to in inflammatory bone destruction remain unclear. Herein, we document that neutrophil extracellular traps (NETs) have a direct role in mediating inflammatory pathology. In an established animal model of periodontitis, we demonstrate that genetic or pharmacologic inhibition of NETs formation, or removal of NETs by DNase-Ⅰ, alleviates inflammatory bone loss in vivo. Investigating the mechanisms by which NETs drive periodontal inflammation, we find that extracellular histones have a direct role in disease progression. Consistent with findings in animal models, histones bearing classic NET-associated post-translational modifications are correlated with disease severity and are significantly elevated in local lesions and systemic circulation of patients with periodontitis. Our work reveals NETs-associated components as pathogenic mediators, potential biomarkers, and therapeutic targets for periodontitis.

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Hydrogen sulfide, a novel small molecule signalling agent, participates in GAs biosynthesis under heat stress and the regulation of multiple signaling pathway genes in Ganoderma lucidum

Project description:As one of the most important environmental factors, heat stress (HS) has been found to affect various biological activities of organisms such as growth, signal transmission, primary metabolism and secondary metabolism. Ganoderma lucidum has become a potential model system for evaluating how environmental factors regulate the secondary metabolism of basidiomycetes. Previous research showed that HS can induce the biosynthesis of ganoderic acids (GAs). In this study, we found the existence of hydrogen sulfide in Ganoderma lucidum; moreover, HS increased GAs biosynthesis and could affect the hydrogen sulfide content. We found that sodium hydrosulfide (NaHS), an exogenous donor of hydrogen sulfide, could revert the increased GAs biosynthesis elicited by HS. This result indicated that an increased content of hydrogen sulfide, within limits, was associated with HS-induced GAs biosynthesis. Our results further showed that the GAs content was increased in CBS-silenced strains and could be reverted to WT strain levels by the addition of NaHS. Transcriptomic analyses indicated that that H2S can affect various intracellular signal pathways and physiological processes in G. lucidum. Further studies showed that H2S could affect the intracellular calcium concentration and thus regulate the biosynthesis of GAs. This study demonstrated that hydrogen sulfide is involved in the regulation of secondary metabolic processes induced by heat stress in filamentous fungi.

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