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

ABSTRACT: 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.

ORGANISM(S): Staphylococcus aureus

PROVIDER: GSE99432 | GEO | 2017/06/19

SECONDARY ACCESSION(S): PRJNA388446

REPOSITORIES: GEO

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Widespread cysteine persulfidation in activated macrophages as a protective mechanism against oxidative-inflammatory stress

Project description:A hallmark of immune-inflammatory responses is the generation of reactive oxygen and nitrogen species by innate immune cells, in particular macrophages. How macrophages cope with excess oxidant production and associated redox stress is not fully understood. Recent evidence implicates reactive sulfur species (RSS) in inflammatory responses, however, how RSS affect macrophage function and its ability to cope with oxidative-inflammatory stress remains poorly understood. Herein, we investigated endogenous pathways of RSS biogenesis and clearance in macrophages, and in particular, explored how hydrogen sulfide (H2S) and thiol persulidation influences macrophage oxidative-inflammatory response. We report that classical activation of mouse or human macrophages with lipopolysaccharide and interferon-γ (LPS/IFN-γ) triggers a marked production of H2S/RSS, leading to a widespread increase in protein persulfidation. Endogenous H2S/persulfidation levels were governed by the activity of the cystine importer xCT, the H2S-generating enzyme cystathionine γ-lyase and the sulfide-metabolizing enzyme sulfide quinone oxidoreductase (SQOR). High levels of H2S/persulfidation, observed upon LPS/IFN-γ stimulation or SQOR inhibition, were associated with a state of increased resistance to oxidative stress. Furthermore, enhanced persulfidation correlated with attenuated activation of the macrophage inflammasome and diminished inflammatory cell death. These findings shed light on the metabolism and effects of RSS in macrophages and point to an important role for persulfides in enabling macrophages to cope with oxidative-inflammatory stress.

2024-05-21 | PXD044043 | Pride

Characterization of Calprotectin treated medium

Project description:The goal of this study is to correlate the transcriptional response of S. aureus cells grown in Calprotectin treated medium with that of cells grown in Mn or Zn depletion conditions. Keywords: RNA sample Staphylcoccus aureus strain Newman was grown to mid-log phase in Calprotectin treated medium or medium lacking either Zn or Mn. RNA was isolated, labeled and hybridized to an S. aureus Affymetrix GeneChip. Biological replicates are indicated as A, B, or C.

2010-05-26 | E-GEOD-9828 | biostudies-arrayexpress

CST interacts with the cohesin complex and promotes chromosome cohesion

Project description:Sister chromatid cohesion (SCC), the pairing of sister chromatids following DNA replication until mitosis, is established by loading of the cohesin complex on newly replicated chromatids. Cohesin must then be maintained until mitosis to prevent segregation defects and aneuploidy. However, how SCC is established and maintained until mitosis remains incompletely understood and emerging evidence suggests that replication stress may lead to premature SCC loss. Here, we report that the single-stranded DNA-binding protein CTC1-STN1-TEN1 (CST) aids in SCC. CST primarily functions in telomere length regulation but also has known roles in replication restart and DNA repair. Following depletion of CST subunits, we observed an increase in the complete loss of SCC. Additionally, we determined that CST associates with the cohesin complex. Unexpectedly, we did not find evidence of altered cohesion or mitotic progression in the absence of CST; however, we did find that treatment with various replication inhibitors increased the association between CST and cohesin. Since replication stress was recently shown to induce SCC loss, we hypothesized that CST may be required to maintain or remodel SCC following DNA replication fork stalling. In agreement with this idea, SCC loss was greatly increased in CST-depleted cells following exogenous replication stress. Based on our findings, we propose that CST aids in the maintenance of SCC at stalled replication forks to prevent premature cohesion loss.

2021-07-28 | PXD026264 | Pride

Anti-inflammatory effects of differential molecular weight hyaluronic acids on UVB-induced calprotectin-mediated keratinocyte inflammation

Project description:Background: The biological functions of HA are related to its molecular weight and binding to its receptor TLR4 or CD44. Recent studies have shown that LMW-HA exhibits proinflammatory effects, while HMW-HA functions as an anti-inflammatory factor. UVB-induced epidermal inflammation is mainly mediated by endogenous molecules, such as DAMPs, that cause severe skin damage by activating TLR signaling pathways. Objective: Since both LMW- and HMW-HA have inhibitory functions on TLR-mediated macrophage inflammation, HA is assumed to suppress UVB-induced DAMP-mediated inflammation in the skin. In this study, both uLMW-HA and HMW-HA were found to inhibit UVB-induced keratinocyte inflammation. Methods: To elucidate whether HAs have anti-inflammatory effects on inflammation induced by UVB exposure, we performed whole transcriptome analysis in HaCaT cells treated with or without HAs after UVB exposure. Results: UV radiation induced upregulation or downregulation of genes (FC>1.2 or FC<0.8, q<0.05) were obtained. We analyzed network of these genes with Ingenuity Pathway analysis using information collected from databases on protein interactions. IL-6 was detected as an upstream factor of HA suppressing UV-radiation effects on HaCaT cells. Canonical pathway analysis also shows uLMW-HA downregulated NF-κB, which is located downstream of TLR4 signaling pathway, although HMW-HA did not show downregulation of NF-κB signaling pathway. Conclusions: Both uLMW-HA and HMW-HA were found to inhibit UVB-induced keratinocyte inflammation.

2022-08-05 | GSE201850 | GEO

Effect of sulfide on growth physiology and gene expression of Desulfovibrio vulgaris Hildenborough

Project description:The effect of sulfide stress on Desulfovibrio vulgaris Hildenborough (DvH) gene expression was determined by comparing the gene expression profiles of DvH under conditions in which sulfide was allowed to accumulate (high sulfide, average concentration 10 mM) against DvH cells grown under conditions in which sulfide was removed by continuous gassing (low sulfide, average concentration 1 mM). High sulfide significantly decreased the instantaneous growth rate constant and final cell density of the culture indicating a decreased bioenergetic fitness. Changes in gene expression caused by exposure to high sulfide were determined using full-genome DvH microarrays. The transcription of ribosomal protein-encoding genes was decreased, in agreement with the lower growth rate of DvH under high sulfide conditions. Interestingly, expression of the gene for DsrD, located downstream of the genes for dissimilatory sulfite reductase (DsrAB) was also strongly down-regulated. In contrast, the expression of many genes involved in iron accumulation, stress response and proteolysis, and chemotaxis were increased. This indicates that high sulfide represents a significant stress condition, in which the bioavailability of metals like iron may be lowered and in which proteins (e.g. metalloenzymes) may need to be refolded, or proteolytically degraded. Overall this leads to a reduced growth rate and less efficient biomass production with available resources. For each condition 2 unique biological samples were hybridized to 4 arrays that each contained duplicate spots. Genomic DNA was used as universal reference.

2010-05-06 | E-GEOD-15073 | biostudies-arrayexpress

Effect of sulfide on growth physiology and gene expression of Desulfovibrio vulgaris Hildenborough

2009-08-18 | GSE15073 | GEO

Gene expression profile of carbon starvation gene knockouts, ÎcstA and ÎyjiY, in Salmonella typhimurium

Project description:Two carbon starvation (cst) genes, cstA and yjiY, in Salmonella are predicted to mediate peptide utilization under nutrient stress. However, the mechanistic details of their function and their importance in the context of Salmonella pathogenesis is not addressed. In this study, the transcriptomes of cst gene knockouts were compared to that of wild type to check the global impact of cst genes on Salmonella metabolism as well as pathogenesis. Microarray was done for duplicate samples for each strain in late log phase of growth in LB, which is also marked by the expression of many virulence associated genes. Organism : Salmonella typhimurium , Agilent Custom Salmonella Typhimurium Gene Expression 8x15k Array (AMADID: 046639) designed by Genotypic Technology Private Limited.

2016-04-01 | E-GEOD-67315 | 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

Gene expression profile of carbon starvation gene knockouts, ΔcstA and ΔyjiY, in Salmonella typhimurium

2016-04-01 | GSE67315 | GEO

The impact of low molecular weight hyaluronan on the lipidomic profile and global gene expression of peripheral blood mononuclear cells in asthma

Project description:Hyaluronan (HA) is the major glycosaminoglycan in the extracellular matrix involved in the pathogenesis of asthma and other chronic inflammatory diseases. During inflammation there is an increased breakdown of HA, resulting in the local and systemic accumulation of low molecular weight (LMW) HA. Eicosanoids, derived from cytosolic phospholipase A2 group IVA activation, are potent lipid mediators also attributed to acute and chronic inflammation. We investigated the effect of LMW HA on lipidomic profile and global gene expression in PBMCs of patients with mild-to-moderate and severe asthma. We found that LMW HA increased production of 68 unique lipid species, among which PGE2, PGA2, PGD2, PGF2a, 15-HETE, TxB2, 11,12-EET, 14,15 EET, 13-HOTrE(y) and 16 (17) EpDPE were significantly upregulated in severe asthmatics. We also performed a systematic genome-wide expression analysis of LMW HA signaling, confirming its highly immunostimulatory potential. However, in severe asthmatics the LMW HA-induced global gene expression profile showed a comprehensive impairment in interferon signaling, cell apoptosis and cell movement, leading to diminished antiviral responses. Likewise, LMW HA-induced production of IL12 p40, CXCL10, CXCL11 and CCL8was markedly reduced in severe asthmatics. Our findings suggest a previously unforeseen link between extracellular matrix, global lipid production and antiviral responses in the pathogenesis of severe asthma. We used microarray to perform a systematic genome-wide expression analysis of LMW HA effect in peripheral blood mononuclear cells in control subjects, mild-to moderate asthma and severe asthma patients

2016-11-14 | GSE59019 | GEO

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