GNPS - Antibiotic Mice Liver data
Ontology highlight
ABSTRACT:
INSTRUMENT(S): maXis
ORGANISM(S): Animalia
SUBMITTER: 
Pieter Dorrestein Quinn
PROVIDER: MSV000083436 | GNPS | Wed Feb 13 10:59:00 GMT 2019
REPOSITORIES: GNPS
Similar Datasets
Project description:These are raw and mzXML files from the PD17-PD36 mice obtained from Raffatellu lab. Mice were given antibiotics and gavaged with glycocholic acid, taurocholic acid, phenylalanacholic acid, leucocholic acid and tyrosocholic acid.
2019-02-13 | MSV000083436 | MassIVE
Project description:These are raw and mzXML data from mice tissue obtained from the Raffatellu lab. This excludes the fecal data collected from the time series.
2019-02-14 | MSV000083446 | MassIVE
Project description:These are raw and mzXML data from mice tissue obtained from the Raffatellu lab. This excludes the fecal data collected from the time series.
2019-02-14 | MSV000083446 | GNPS
Project description:Tan2012 - Antibiotic Treatment, Inoculum Effect
The efficacy of many antibiotics decreases with increasing bacterial density, a phenomenon called the ‘inoculum effect’ (IE). This study reveals that, for ribosome-targeting antibiotics, IE is due to bistable inhibition of bacterial growth, which reduces the efficacy of certain treatment frequencies.
This model is described in the article:
The inoculum effect and band-pass bacterial response to periodic antibiotic treatment.
Tan C, Phillip Smith R, Srimani JK, Riccione KA, Prasada S, Kuehn M, You L.
Mol Syst Biol. 2012 Oct 9; 8:617
Abstract:
The inoculum effect (IE) refers to the decreasing efficacy of an antibiotic with increasing bacterial density. It represents a unique strategy of antibiotic tolerance and it can complicate design of effective antibiotic treatment of bacterial infections. To gain insight into this phenomenon, we have analyzed responses of a lab strain of Escherichia coli to antibiotics that target the ribosome. We show that the IE can be explained by bistable inhibition of bacterial growth. A critical requirement for this bistability is sufficiently fast degradation of ribosomes, which can result from antibiotic-induced heat-shock response. Furthermore, antibiotics that elicit the IE can lead to 'band-pass' response of bacterial growth to periodic antibiotic treatment: the treatment efficacy drastically diminishes at intermediate frequencies of treatment. Our proposed mechanism for the IE may be generally applicable to other bacterial species treated with antibiotics targeting the ribosomes.
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and identified by: MODEL1208300000
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To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
2024-09-02 | BIOMD0000000425 | BioModels
Project description:Antibiotics have long-lasting consequences on the gut microbiota with the potential to impact host physiology and health. However, little is known about the transgenerational impact of an antibiotic-perturbed microbiota. Here we demonstrated that adult pregnant female mice inoculated with a gut microbial community shaped by antibiotic exposure passed on their dysbiotic microbiota to their offspring. This dysbiotic microbiota remained distinct from controls for at least 5 months in the offspring without any continued exposure to antibiotics. By using IL-10 deficient mice, which are genetically susceptible to colitis, we showed mice that received an antibiotic-perturbed gut microbiota from their mothers had increased risk of colitis. Taken together, our findings indicate that the consequences of antibiotic exposure affecting the gut microbiota can extend to a second generation.
2017-12-01 | GSE92623 | GEO
Project description:RNA-Seq of livers from aged mice exposed to antibiotics
2021-07-25 | GSE154465 | GEO
Project description:Mice with mitochondrial complex I deficiency (Ndufs4-/-) suffer from severe energy impairment primarily affecting the brain and die at P55. A small molecule screen developed by our lab using cells harboring human mitochondrial disease mutations identified antibiotics targeting mitochondrial translation as potent inhibitors of cell death under nutrient stress conditions. Doxycycline, which was identified amongst these antibiotics, was administered in the diet of Ndufs4-/- mice after weaning at P21. Mice fed with doxycycline showed improved motor function and significantly increased lifespan relative to untreated Ndufs4-/- mice. In order to investigate the molecular changes promoted by doxycycline in the brains of these mice, Ndufs4-/- doxycycline treated (DOX), Ndufs4-/- untreated (KO), and Ndufs4+/+ (WT) control mice were sacrificed at P55 and their brains harvested. Proteomic analysis revealed doxycycline treatment largely prevented the neuroimmune and inflammatory profile identified in the Ndufs4-/- mice. These findings implicate a potentially causality of these proteins in the neuronal cell death ultimately leading to the observed brain pathology.
2021-09-09 | PXD022860 | Pride
Project description:Antibiotic therapy causes changes in bacterial abundance and metabolism within the gut microbiome. These changes can lead to complications in the host such as microbiome dysbiosis and opportunistic infections. Additionally, increasing multidrug resistance causes significant morbidity and mortality in patients with bacterial infections. Bacteroides thetaiotaomicron (Bth) is both a normal commensal in the gut and an opportunistic pathogen in other body sites. Our lab has shown that -lactam treatment in mice decimates nearly all gut bacterial species except Bth, which experiences a bloom. We propose that in the gut, Bth enters a protected state linked to metabolic changes such as an increase in stress response and polysaccharide fermentation, and a decrease in hexose utilization. Bth is also protected from -lactams in vitro when grown on fiber as opposed to glucose. The goal of this project is to understand what mechanism is responsible for this polysaccharide-mediated tolerance (PM-tolerance). Studies of other bacteria show that an increase in respiratory metabolism independent of growth rate promotes susceptibility to bactericidal antibiotics. Bth has a diverse array of metabolic machinery including an electron transport chain (ETC) that works under anaerobic or microaerobic conditions. Transcriptional analysis of Bth treated with the -lactam amoxicillin revealed a decrease in ETC enzyme expression when given fiber vs glucose. We found that knocking out different ETC enzymes alters the PM-tolerance phenotype in vitro. Thus, it appears that respiratory capacity is linked to -lactam susceptibility in Bth. This work improves upon our understanding of bacterial tolerance strategies and could help identify future therapeutic targets to combat multidrug resistance.
2024-07-20 | GSE251676 | GEO
Project description:The early life microbiome plays important roles in host immunological and metabolic development. Because type 1 diabetes (T1D) incidence has been increasing substantially in recent decades, we hypothesized that early-life antibiotic use alters gut microbiota that predisposes to disease. Using NOD mice that are genetically susceptible to T1D, we examined the effects of exposure to either continuous low-dose antibiotics or pulsed therapeutic antibiotics (PAT) early in life, mimicking childhood exposures. We found that in mice receiving PAT, T1D incidence was significantly higher, microbial community composition and structure differed compared with controls. In pre-diabetic male PAT mice, the intestinal lamina propria had lower Th17 and T reg proportions and intestinal SAA expression than in controls, suggesting key roles in transducing the altered microbiota signals. PAT affected microbial lipid metabolism and host cholesterol biosynthetic gene expression. These findings show that early-life antibiotic treatments alter the gut microbiota and its metabolic capacities, intestinal gene expression, and T-cell populations, accelerating T1D onset in NOD mice.
2016-05-20 | GSE81648 | GEO
Project description:We performed RNA-seq experiments to compare the gene expression profiles of cells expressing single-codon substitutions in the antibiotic resistance genes NDM-1, CAT-I, or aadB in the absence of antibiotics. Mutations with deleterious fitness effects in the absense of antibiotics also caused significant changes in gene expression in a number of genes related to stress-response pathways including the regulator of colanic acid capsule synthesis (Rcs) response, the phage shock protein response (Psp), and the oxidative stress response. Fold differences in gene expression were mutation- and gene-dependent.
2022-12-31 | GSE199248 | GEO