Interpersonal variability in gut microbial calprotectin metabolism
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB52930 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR9752610.fastq.gz | Fastqsanger.gz | |||
| ERR9752620.fastq.gz | Fastqsanger.gz | |||
| ERR9752611.fastq.gz | Fastqsanger.gz | |||
| ERR9752621.fastq.gz | Fastqsanger.gz | |||
| ERR9752612.fastq.gz | Fastqsanger.gz |
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Project description: Not available
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Project description:The intestines house a diverse microbiota that must compete for nutrients to survive, but the specific limiting nutrients that control pathogen colonization are not clearly defined. Clostridioides difficile colonization typically requires prior disruption of the microbiota, suggesting that outcompeting commensals for resources is key in establishing C. difficile infection (CDI). The immune protein calprotectin (CP) is released into the gut lumen during CDI to chelate zinc (Zn) and other essential nutrient metals. Yet, the impact of Zn limitation on C. difficile colonization is unknown. To define C. difficile responses to Zn limitation, we performed RNA sequencing on C. difficile exposed to CP. In media with CP, C. difficile upregulated genes involved in metal homeostasis and amino acid metabolism.
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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
Project description:Morphine and its pharmacological derivatives are the most prescribed analgesics for moderate to severe pain management. However, chronic use of morphine reduces pathogen clearance and induces bacterial translocation across the gut barrier. The enteric microbiome has been shown to play a critical role in the preservation of the mucosal barrier function and metabolic homeostasis. Here, we show for the first time, using bacterial 16s rDNA sequencing, that chronic morphine treatment significantly alters the gut microbial composition and induces preferential expansion of the gram-positive pathogenic and reduction of bile-deconjugating bacterial strains. A significant reduction in both primary and secondary bile acid levels was seen in the gut, but not in the liver with morphine treatment. Morphine induced microbial dysbiosis and gut barrier disruption was rescued by transplanting placebo-treated microbiota into morphine-treated animals, indicating that microbiome modulation could be exploited as a therapeutic strategy for patients using morphine for pain management. In this study, we establish a link between the two phenomena, namely gut barrier compromise and dysregulated bile acid metabolism. We show for the first time that morphine fosters significant gut microbial dysbiosis and disrupts cholesterol/bile acid metabolism. Changes in the gut microbial composition is strongly correlated to disruption in host inflammatory homeostasis13,14 and in many diseases (e.g. cancer/HIV infection), persistent inflammation is known to aid and promote the progression of the primary morbidity. We show here that chronic morphine, gut microbial dysbiosis, disruption of cholesterol/bile acid metabolism and gut inflammation; have a linear correlation. This opens up the prospect of devising minimally invasive adjunct treatment strategies involving microbiome and bile acid modulation and thus bringing down morphine-mediated inflammation in the host.
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Project description:Calprotectin (CP) inhibits bacterial viability through extracellular chelation of transition metals. However, how CP influences general metabolism remains largely unexplored. We show here that CP restricts bioavailable Zn and Fe to the pathogen Acinetobacter baumannii, inducing an extensive multi-metal perturbation of cellular physiology. Detailed here are the RNA sequencing files of WT A. baumannii ATCC 17978 grown plus or minus recombinant human calprotectin.
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Project description:Variability in gene expression is an important and largely unknown phenomenon responsible of tumor resistance to chemotherapy. Here, we show that energy metabolism proteins are highly variable, specially Glut1, G6PD, PKM2 and SDHA. In contrast, the variability of housekeeping proteins was low. We identified the PI3K/Akt/mTor pathway as the source of variability for PKM2.Variability was independent of the energy source used. However, cells grown on glucose down-regulate G6PDH and SDHA, promoting oxidative stress. Variability and chemotherapy plasticity were directly related, and the combination of drugs with opposite effect on the expression of plastic proteins resulted in positive synergy. Human solid tumor cells displayed higher variability in metabolic enzymes than cultured cells. The most aggressive tumors showed higher variability than less aggressive ones. This suggests that variability in energy metabolism enzymes could be a biomarker for tumor stratification and therapy election.
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Project description:The host protein calprotectin inhibits the growth of a variety of bacterial pathogens through metal sequestration in a process known as 'nutritional immunity'. Staphylococcus aureus growth is inhibited by calprotectin in vitro and calprotectin is localized in vivo to staphylococcal abscesses during infection. However, the staphylococcal adaptations that provide defense against nutritional immunity and the role of metal-responsive regulators are not fully characterized. In this work, we define the transcriptional response of S. aureus and the role of the metal-responsive regulators, Zur, Fur, and MntR, in response to metal limitation by calprotectin exposure. Additionally, we identified genes affecting the fitness of S. aureus during metal limitation through a Transposon sequencing (Tn-seq) approach. Loss of function mutations in clpP, which encodes a proteolytic subunit of the ATP-dependent Clp protease, demonstrate reduced fitness of S. aureus to the presence of calprotectin. ClpP contributes to pathogenesis in vivo in a calprotectin-dependent manner. These studies establish a critical role for ClpP to combat metal limitation by calprotectin and reveal the genes required for S. aureus to outcompete the host for metals.
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Project description:Variability in energy metabolism enzymes in tumor cells.
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Project description:Gut microbiota are known to influence oral drug disposition, yet the specific host pathways they affect remain poorly characterized. This study provides a transcriptome-wide characterization of how physiological gut microbiota regulate the expression of intestinal transporters, phase I and phase II metabolic enzymes, and barrier machinery relevant to oral drug disposition. By identifying microbiota-responsive processes, this work defines the scope of inter-individual variability attributable to gut microbial effects.
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