Ontology highlight
ABSTRACT:
PROVIDER: PRJNA938186 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23605000_1.fastq.gz | Fastqsanger.gz | |||
| SRR23605000_2.fastq.gz | Fastqsanger.gz | |||
| SRR23605001_1.fastq.gz | Fastqsanger.gz | |||
| SRR23605001_2.fastq.gz | Fastqsanger.gz | |||
| SRR23605002_1.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: Gut microbiota-derived metabolites play a pivotal role in the maintenance of local gut homeostasis and can even induce systemic effects via accumulation in the bloodstream. Here, we demonstrate that mono-colonization of germ-free (GF) mice with Clostridium sporogenes protects mice from inflamation and death induced by DSS colitis. Method: 8-12-week-old male mice (GF, SPF and GF colonized with C. sporogenes (CS)) were treated with 2.5% DSS in drinking water for 5 days and colon tissue was isolated on day 7. RNA was isolated from the colon tissue and RNA sequenzing was performed. Results: Mono-colonization of GF mice with Clostridium sporogenes protected the mice from DSS colitis induced death, while producing high amounts of indole-3-propionic acid (IPA), branched chain (BCFA) and short-chain (SCFA) fatty acids. In comparison to CS mice, SPF mice showed much higher levels of inflammatory related genes and a worse histological score. Conclusion: Histological stainings and the RNAseq both showed high levels of protection of C. sporogenes colonized mice in colitis, compared to SPF and GF animals. The data provide evidence for a therapeutic potential of C. sporogenes for IBD patients.
2024-10-15 | GSE264024 | GEO
Project description:Cigarette smoke (CS)-induced airway inflammation is an important pathologic feature of chronic obstructive pulmonary disease (COPD). Recent studies suggest a potential role of JunD in the regulation of inflammation, but its role in CS-induced airway inflammation has not been reported. This study aimed to determine its role in CS-induced airway inflammation through bioinformatics analysis and in vitro and in vivo experiments. Data from the Gene Expression Omnibus (GEO) database (GSE37147) were analyzed using weighted gene co-expression network analysis (WGCNA) and key driver analysis (KDA), and these analyses were validated using the GSE47460 dataset. The effect of CS on JunD expression was examined in lung tissues of COPD patients and CS-exposed mice and in CS extract (CSE)-exposed BEAS-2B cells. The effects of CSE on airway epithelial inflammatory injury after JunD knockdown or overexpression were also investigated. mRNA-seq and chromatin immunoprecipitation (ChIP)-seq were used to explore the mechanism of JunD-mediated CS-induced airway inflammation. Mice were injected with adeno-associated virus serotype 9 (AAV9)-JunD vector or control vector and then exposed to CS for 4 weeks, and lung tissue morphology and airway inflammation were evaluated. KDA of the lung function-related gene modules in GSE37147 revealed a potential role of JunD in COPD, which was validated in GSE47460. JunD was downregulated in lung tissues of COPD patients and CS-exposed mice and in BEAS-2B cells. JunD knockdown aggravated CSE-induced tumor necrosis factor (TNF)-α and interleukin (IL)-1β release by BEAS-2B cells, while JunD overexpression attenuated these effects. mRNA-seq and ChIP-seq identified several JunD-regulated genes, which are involved in the immune response and TNF signaling pathway and are commonly dysregulated in cell models of airway inflammation. In vivo, JunD overexpression attenuated the CS-induced inflammatory cell infiltration and inflammatory cytokine release in mouse lungs. Thus, JunD is involved in CS-induced airway inflammation and JunD-based therapy may be useful in CS-induced airway disorders.
2020-12-09 | GSE162902 | GEO
Project description:Cesium (Cs+) is a potentially toxic mineral element that is released into the environment and taken up by plants. Although Cs+ is chemically similar to potassium (K+), and much is known about K+ transport mechanisms, it is not clear through which K+ transport mechanisms Cs+ is taken up by plant roots. In this study, the role of AtHAK5 in high affinity K+ and Cs+ uptake was characterized. It is demonstrated that AtHAK5 is localized to the plasma membrane under conditions of K+ deprivation, when it is expressed.
2010-04-20 | GSE20222 | GEO
Project description:Stress is a powerful modulator of neuroendocrine, behavioral, and immunological functions. So far, the molecular mechanisms of response to stressors still remain elusive. In the current study, after 10 days of repeated chronic stress (hot-dry environment and electric foot-shock), a murine model of combinedstress (CS) was created in the SPF Wistar rats. Meanwhile, we established an ulcerative-colitis (UC) rat model induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS)/ethanol enema according to previous studies. The blood, hypothalamus, and colon tissues of these rats from CS, normal control (NC), UC and sham (SH) groups, were collected for further investigations. Comparing to the NC group, the serum levels of T3, T4, fT3 and fT4 were obviously decreased in the CS group after chronic stress, indicating that thyroid dysfunction was induced by long-term combined stress. Moreover, the application of RNAseq and subsequent analyses revealed that neurological disorder and immunosuppression were also caused in the hypothalamus and colon tissues, respectively. Comparing with SH group, besides the induced colon infammation, thyroid dysfuntion and neurological disorder were also produced in the UC group, suggesting that hypothalamic-pituitary-thyroid (HPT) axis and gastrointestinal system might not function in isolation, but rather, have intricate crosstalks.
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Project description:This study investigated whether mitochondria-targeted peptide SS-31 played a protective role in cigarette smoke (CS)-induced airway inflammation and oxidative stress in mice. Mice were exposed to CS for 4 weeks to establish a CS-induced airway inflammation model, then treated with SS-31. Pathological changes and oxidative stress in lung tissue, inflammatory cell counts and pro-inflammatory cytokines in bronchoalveolar lavage fluid (BALF) were examined. RNA sequencing from lung tissue and western blotting were conducted to investigate mechanisms. SS-31 attenuated CS-induced inflammatory injury of the airway. Numbers of total cells, neutrophils, and macrophages and levels of tumor necrosis factor α, interleukin 6, and matrix metallopeptidase 9 in BALF were markedly reduced by SS-31. SS-31 attenuated CS-induced oxidative stress by decresing malondialdehyde and myeloperoxidase levels, and increasing superoxide dismutase activity. It also reversed the expression of mitochondrial fission protein and optic atrophy 1 protein, and reduced cytochrome c release into the cytosol. RNA sequencing revealed that SS-31 changed CS-induced expression profiles and enriched MAPK pathway, western blotting confirmed that SS-31 inhibited the CS-activated MAPK pathway. SS-31 alleviates CS-induced airway inflammation and oxidative stress, possibly via the regulation of mitochondrial function and MAKP pathway, SS-31 may be a novel drug for CS-induced airway disorders.
2020-12-25 | GSE163835 | GEO
Project description:Our study aimed to identify miRNAs expression of which is affected by exposure to cigarette smoke (CS) in alveolar type-II cells. Identification and delineation of their modes of action is important for understanding CS-induced failure of repair mechanisms in COPD pathogenesis
2020-05-01 | GSE131188 | GEO
Project description:At high concentrations ceasium (Cs) is toxic to plant growth. This toxic effect may occur when Cs blocks potassium (K) uptake mechanisms in plants. Consequently, plants starved of K and plants exposed to toxic concentrations of Cs should have similar gene expression patterns. To test this hypothesis, Arabidopsis will initially be grown on agar containing 1/10 MS salts before being transferred to either 1/10 MS nutrient solution (control plants), 1/10 MS nutrient solution containing 2 mM Cs, or 1/10 MS nutrient solution with no K. Roots and shoot will then be harvested seven days after transfer and used to challenge ATH1 GeneChips. Keywords: compound_treatment_design
2007-01-08 | GSE6160 | GEO
Project description:Chronic obstructive pulmonary disease (COPD) is characterized by a progressive decline in lung function, caused by exposure to exogenous particles, mainly cigarette smoke (CS). COPD pathogenesis is initiated and perpetuated by an abnormal CS-induced inflammatory response of the lungs, involving both innate and adaptive immunity. Specifically, B cells organized in iBALT structures, as well as macrophages, accumulate in the lungs and contribute to CS-induced emphysema, but the mechanisms thereof remain unclear. Here, we demonstrate that B cell-deficient mice are significantly protected against CS-induced emphysema. Chronic CS exposure led to increased lung compliance, total lung capacity, and mean linear chord length in WT, but not B cell-deficient mice, associated with an increased size and number of iBALT structures. The increased accumulation of macrophages around iBALT and in emphysematous alveolar areas in CS-exposed WT mice coincided with upregulated MMP12 expression. In vitro co-culture experiments using B cells and macrophages demonstrated that B cell-derived IL-10 drives macrophage activation and MMP12 upregulation. In summary, B cell function in iBALT formation in CS-induced emphysema provides a new innovative mechanism, which could be explored as a target for therapeutic intervention in COPD patients.
2014-12-04 | GSE52509 | GEO
Project description:We investigated the root growth of several knockout mutants of heat shock protein family genes and found that heat stress response was compromised in these mutants compared to wild type plants. It suggested that heat shock protein genes including heat shock protein genes including HSP17s, HSP23s, HSP101, and HSFA2 proteins are deployed upon exposure to Cs for plant stress tolerance. Our study provided novel insights into the molecular events occurring in Cs-stressed plants.
2024-04-06 | GSE262902 | GEO