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Hydrogen sulfide stimulates Mycobacterium tuberculosis respiration and growth to exacerbate TB disease

ABSTRACT: Hydrogen sulfide stimulates Mycobacterium tuberculosis respiration and growth to exacerbate TB disease

PROVIDER: PRJEB35872 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3770570_1.fastq.gz	Fastqsanger.gz
	ERR3770570_2.fastq.gz	Fastqsanger.gz
	ERR3770571_1.fastq.gz	Fastqsanger.gz
	ERR3770571_2.fastq.gz	Fastqsanger.gz
	ERR3770572_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Hydrogen sulfide stimulates Mycobacterium tuberculosis respiration and growth to exacerbate TB disease

Project description:The aim of this experiment was to determine how exposure of Hydrogen sulfide impacts gene expression in Mycobacterium tuberculosis. RNA was isolated from actively growing mycobacterial cells (0.6-0.8 OD600) using Trizol according to established protocols (27). Briefly, cells were exposed to 25 µM GYY4137 for 1 hr under carefully controlled conditions (n=3/group) and RNA isolated. Unexposed cells received spent GYY4137 (without any capacity to produce Hydrogen sulfide).

2020-01-04 | E-MTAB-7421 | biostudies-arrayexpress

Hydrogen sulfide stimulates Mycobacterium tuberculosis respiration, growth and pathogenesis.

Project description:Hydrogen sulfide (H2S) is involved in numerous pathophysiological processes and shares overlapping functions with CO and •NO. However, the importance of host-derived H2S in microbial pathogenesis is unknown. Here we show that Mtb-infected mice deficient in the H2S-producing enzyme cystathionine β-synthase (CBS) survive longer with reduced organ burden, and that pharmacological inhibition of CBS reduces Mtb bacillary load in mice. High-resolution respirometry, transcriptomics and mass spectrometry establish that H2S stimulates Mtb respiration and bioenergetics predominantly via cytochrome bd oxidase, and that H2S reverses •NO-mediated inhibition of Mtb respiration. Further, exposure of Mtb to H2S regulates genes involved in sulfur and copper metabolism and the Dos regulon. Our results indicate that Mtb exploits host-derived H2S to promote growth and disease, and suggest that host-directed therapies targeting H2S production may be potentially useful for the management of tuberculosis and other microbial infections.

| S-EPMC6987094 | biostudies-literature

Transcriptomic study of hydrogen sulfide toxicity in Methylococcus capsulatus

Project description:Stress response of Methylococcus capsulatus str.Bath toward hydrogen sulfide (H2S) was investigated via physiological study and transcriptomic profiling. M. capsulatus (Bath) can grow and tolerate up to 0.75%vol H2S in headspace. Vast change in pH suggests biological relevant sulfide oxidation. Dozens of H2S-sensitive genes were identified from comparison of cell transcriptome in different H2S concentrations. Mc sulfide quinone reductase (SQR) and persulfide dioxygenase were found to be active during sulfide detoxification. Moreover, xoxF, a novel lanthanide(Ln)-dependent methanol dehydrogenase (MDH) was overexpressed in H2S while mxaF, a calcium-dependent MDH, was down-regulated, and such MDH switch phenomenon is also well known to be induced by addition of lanthanide via an as-yet-unknown mechanism. Activities in quorum sensing and RND efflux pump also suggest their role in sulfide detoxification, and might provide insight on the xoxF/mxaF switch mechanism.

2021-12-24 | GSE192351 | GEO

relationship between the level of plasma hydrogen sulfide in the patients with colorectal cancer

Project description:Interventions: Case series:nill;The control group:nill Primary outcome(s): Hydrogen sulfide;Pathological diagnosis Study Design: Case-Control study

| 2671665 | ecrin-mdr-crc

Hydrogen sulfide (H2S) modulates lifespan of C.elegans

Project description:Hydrogen sulfide (H2S) is formed naturally from L-cysteine in a variety of mammalian and non-mammalian cells. To date, numerous biological effects have been ascribed to H2S including control of cardiovascular, immune and nervous function. Over or under production of H2S has been observed in several disease states including hypertension and inflammation. In addition, it has been stipulated that H2S may affect the ageing process. The model nematode Caenorhabditis elegans is ideally suited for assessing drug effects on lifespan since it is relatively short-lived, can be easily exposed to drugs and its genome is fully sequenced and widely annotated.

2013-07-30 | GSE16975 | GEO

The Global Transcriptional Response of Fission Yeast to Hydrogen Sulfide

Project description:Hydrogen sulfide (H2S) as an important gasotransmitter has fundamental roles in human diseases. The cellular effect of H2S has received lots of attention recently. H2S can affect ion channels, transcription factors and kinase in mammals. The mechanism of cellular effect of H2S is not completely understood. We used fission yeast as a model organism to study the global transcriptional profile in response to H2S by microarray.

2012-06-15 | GSE30025 | GEO

Hydrogen sulfide (H2S) modulates lifespan of C.elegans

2013-07-30 | E-GEOD-16975 | biostudies-arrayexpress

Changes in relative transcript amounts caused by hydrogen sulfide treatment, deletion of BigR, and BigR mutant complement in Acinetobacter baumannii

Project description:Acinetobacter baumannii is an opportunistic nosocomial pathogen that is the causative agent of several serious infections in humans. Here, we investigate the response of A. baumannii toward sodium sulfide (Na2S), known to be associated with some biofilms at oxic/anoxic interfaces, as a model for how this major human pathogen manages sulfide homeostasis. These results reveal that A. baumannii encodes two persulfide‑sensing transcriptional regulators, a primary sigma54‑dependent transcriptional activator (FisR), and a secondary system controlled by the persulfide‑sensing repressor biofilm growth‑associated repressor (BigR) both of which regulate operons encoding for sulfide detoxification or transportation. In addition, sulfide induces an alternative cytochrome bd oxidase which is refractory to inhibition by H2S and represses importers of alternate sulfur sources. Lastly, our results suggest additional genes regulated by BigR beyond sulfide detoxification including genes associated with assembly of type 1 chaperone-usher pilus.

2020-06-15 | GSE148264 | GEO

Mapping of hydrogen sulfide molecular targets in human keratinocytes

Project description:In the present paper, we report on the pan-genomics and pan-proteomics analysis of cultured epithelial sheets of human keratinocyte progenitors. Our results notably show that NaHS stimulates the secretion of specific pro-inflammatory cytokines and promotes the synthesis of molecules involved in antioxidative mechanisms

2020-07-29 | GSE148985 | GEO

Changes in relative transcript amounts caused by hydrogen sulfide treatment, calprotectin treatment, and deletion of CstR in Staphylococcus Aureus

Project description:The Staphylococcus aureus strain Newman uses the dithiol-containing repressor CstR to sense sulfide stress via reactive sulfur species (RSS), allowing transcription of a mitochondrial-like sulfide oxidation system, the core of which is genetically linked to methicillin resistance determinants in MRSA strains. The cytoplasm maintains an excess of reduced relative to oxidized low molecular weight (LMW) thiols that are protective against oxidative stress and transition metal (Zn, Cd and Cu) toxicity, buffering these ions to low “free” concentrations via formation of coordination complexes. We hypothesize that unregulated H2S perturbs the LMW thiol pool by generating RSS; these, in turn, react with CstR cysteines (C31, C60), induce cst derepression, and are cleared by cst-encoded enzymes. These results show that sulfide stress induces the cst operon and a zinc starvation response, represses cysteine biosynthesis, and generally represses genes that are induced by acute oxidative stress; in addition, strong repression of the expression of staphylococcal virulence factors is observed in the ∆cstR strain.

2017-06-19 | GSE99432 | GEO

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