Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6898309_1.fastq.gz | Fastqsanger.gz | |||
| SRR6898309_2.fastq.gz | Fastqsanger.gz |
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Project description:Hypersensitivity reactions are rare, but potentially severe adverse effects of sulfonamide antibiotics. Increased in vitro toxicity of lymphocytes, primarily CD8+ T cells, to sulfonamide drug metabolites as been proposed as a marker for sulfonamide hypersensitivity, but the mechanisms underlying this marker are unknown. Therefore, we used microarrays to compare RNA expression of CD8+ T cell-enriched peripheral blood mononuclear cells of human patients who have had a hypersensitivity (HS) reaction to sulfonamide antibiotics vs. patients who have been tolerant (TOL) to a course of sulfonamide antibiotics.
2017-06-26 | GSE100443 | GEO
Project description:Potentiated sulfonamide antibiotics such as trimethoprim/sulfamethoxazole (cotrimoxazole or TMP/SMX) remain the drugs of choice for treatment and prevention of Pneumocystis jiroveci pneumonia, toxoplasma encephalitis, and Isospora infections in HIV infection (aidsinfo.nih.gov). However, HIV-infected patients show a markedly increased risk of delayed hypersensitivity (HS) reactions to TMP/SMX (20-57% incidence) when compared to the general population (3% incidence). The typical manifestation is maculopapular rash with or without fever, and TMP/SMX is the most common cause of cutaneous drug reactions in HIV-infected patients TMP/SMX can also lead to thrombocytopenia, hepatotoxicity, and bullous skin eruptions in more severely affected patients. The risk of sulfonamide HS increases with progression to AIDS, with higher risk seen at lower CD4+ counts. This risk has been attributed, at least in part, to acquired alterations in SMX drug disposition in HIV infection. We hypothesized that HIV infection leads to impaired hepatic SMX detoxification or enhanced SMX bioactivation pathways, which may contribute to the increased incidence of sulfonamide HS. We addressed this question using liver tissue from SIVmac239-infected macaques, a well accepted model of HIV infection. The aim of this study was to evaluate differences in the hepatic expression and activity of SMX biotransformation pathways from drug naïve SIV-infected macaques compared to sex- and age-matched uninfected controls.
2017-07-11 | GSE87158 | GEO
Project description:Freshwater environments such as rivers receive effluent discharges from wastewater treatment plants, representing a potential hotspot for antibiotic resistance genes (ARGs). These effluents also contain low levels of different antimicrobials including biocides and antibiotics such as sulfonamides that can be frequently detected in rivers. The impact of such exposure on ARG prevalence and microbial diversity of riverine environment is unknown, so the aim of this study was to investigate the release of a sub-lethal concentration (<4 g L-1) of the sulfonamide compound sulfamethoxazole (SMX) on the river bacterial microbiome using a microflume system. This system was a semi-natural in-vitro microflume using river water (30 L) and sediment, with circulation to mimic river flow. A combination of ‘omics’ approaches were conducted to study the impact of SMX exposure on the microbiomes within the microflumes. Metaproteomics did not show differences in ARGs expression with SMX exposure in water.
2021-07-06 | PXD023822 | Pride
Project description:Staphylococcus aureus has been shown to cause various types of tissue and systemic infections in humans and livestock with the mortality rate of 20-30%. Some isolates can be highly resistant to antibiotics hence the need to identify better drugs and drug targets. Previous studies have shown that (E)-N-(4-Fluorophenyl)-2-phenylethene sulfonamide (FPSS) could inhibit activities of a bacteria-specific transcription factor sigma B. Sigma B regulons in Bacillus subtilis and in Listeria monocytogenes, including virulence factor genes in L. monocytogenes, were decreased. Since sigma B is also presented in S. aureus, we initially postulated the use of FPSS to target S. aureus sigma B activity and to attenuate its virulence gene expression. Surprisingly, qRT-PCR results revealed that FPSS induced expression of sigma B-dependent gene asp23. RNAseq results showed 39 S. aureus genes were affected by FPSS (37 genes were downregulated and two genes were upregulated). FPSS had no effect on expression of sigB operon in S. aureus.
2025-04-21 | GSE253363 | GEO
Project description:<p>Background: The use of sulfonamides (SAs) caused residual pollution in the environment. Bacteria play an important role in the degradation of sulfonamide antibiotics, and microbial consortium offers advantages over single bacterium. However, the complex degradation process and interaction mechanisms within such consortiums still poorly understood. </p><p>Results: Here, a consortium named ACJ, consisting of Leucobacter sp. HA-1, Bacillus sp. HC-1 and Gordonia sp. HAEJ-1, obtained from activated sludge of pharmaceutical plants, was identified as capable of degrading various SAs. Several papers failed to get the pure culture of Leucobacter sp. in the degradation of SAs, here we successfully obtained the Leucobacter sp. HA-1 pure culture involved in the degradation of SAs with the growth factors provided by strain HC-1 or HAEJ-1. Strain HA-1 was responsible for the initial attack of sulfonamide molecules resulting in the release of 2-aminoquinoxaline (2-AQ) and trihydroxybenzene (HHQ), which were further degraded and used for growth by strain HAEJ-1. Genomic, metabolomic and transcriptomic analyses revealed genes associated with nucleotide repair, ABC transporters, quorum sensing, TCA cycle and cell cycle in strain HA-1 were up-regulated during co-culture compared without the other two strains, which indicated that HA-1 utilized certain factors from strain HC-1 or HAEJ-1 for growth. </p><p>Conclusion: These results revealed that there was a bidirectional ecological relationship of cross-feeding and co-degradation among consortium ACJ. In summary, this study provides new insights into the mechanisms of microbial consortium interaction and co-degradation in antibiotic-contaminated environments.</p>
2024-11-08 | MTBLS11473 | MetaboLights
Project description:ADH5 encodes for the protein GSNOR, an alchol dehydrogenase acting as a denitrosylase. GSNOR reduces S-nitrosoglutathione (GSNO) to an unstable intermediate, S-hydroxylaminoglutathione, which then rearranges to form glutathione sulfonamide, or in the presence of GSH, forms oxidized glutathione (GSSG) and hydroxylamine
2022-12-21 | GSE211114 | GEO