Agilent_E. coli O157 response to Chrysanthemum herba
Ontology highlight
ABSTRACT:
ORGANISM(S): Escherichia coli
PROVIDER: GSE26017 | GEO | 2010/12/14
SECONDARY ACCESSION(S): PRJNA135481
REPOSITORIES: GEO
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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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2024-09-02 | BIOMD0000000425 | BioModels
Project description:Secondary bacterial infections (SBIs) exacerbate influenza-associated disease and mortality. Antimicrobial agents can reduce the severity of SBIs, but many have limited efficacy or cause adverse effects. Thus, new treatment strategies are needed. Kinetic models describing the infection process can help determine optimal therapeutic targets, the time scale on which a drug will be most effective, and how infection dynamics will change under therapy. To understand how different therapies perturb the dynamics of influenza infection and bacterial coinfection and to quantify the benefit of increasing a drug’s efficacy or targeting a different infection process, I analyzed data from mice treated with an antiviral, an antibiotic, or an immune modulatory agent with kinetic models. The results suggest that antivirals targeting the viral life cycle are most efficacious in the first 2 days of infection, potentially because of an improved immune response, and that increasing the clearance of infected cells is important for treatment later in the infection. For a coinfection, immunotherapy could control low bacterial loads with as little as 20 % efficacy, but more effective drugs would be necessary for high bacterial loads. Antibiotics targeting bacterial replication and administered 10 h after infection would require 100 % efficacy, which could be reduced to 40 % with prophylaxis. Combining immunotherapy with antibiotics could substantially increase treatment success. Taken together, the results suggest when and why some therapies fail, determine the efficacy needed for successful treatment, identify potential immune effects, and show how the regulation of underlying mechanisms can be used to design new therapeutic strategies.
Model is encoded by Ruby and submitted to BioModels by Ahmad Zyoud
2020-04-02 | MODEL1812040005 | BioModels
Project description:Chrysanthemum is a garden plant with good economic benefit and high ornamental value. Chrysanthemum in the key period of flowering in autumn and winter, vulnerable to cold damage, affecting the normal growth of the chrysanthemum plant and even death. little is known regarding the study of histone crotonylation in plant cold response. In this study, we first obtained reference chrysanthemum transcriptome data via RNA sequencing. Next, we quantitatively investigated the chrysanthemum proteome, crotonylation, and the association between them in chrysanthemum following low temperature. In total, 365669 unigenes, 6693 proteins and 2017 crotonylation sites were quantified under low temperature stress. There were 24631 up-regulated and 22648 down-regulated unigenes (absolute log2-fold change > 1 and P value<0.05), 393 up-regulated and 500 down-regulated proteins using a 1.2-fold threshold (P<0.05). The lysine crotonylation mainly influenced in photosynthesis, ribosome, antioxidant enzyme and ROS system. In the process of low temperature, 61 lysine crotonylation sites in 89 proteins were up-regulated and 87 lysine crotonylation sites in 72 proteins are down-regulated (1.2-fold threshold, P<0.05).
2021-01-04 | PXD010297 | Pride
Project description:Gene expression analysis of chrysanthemum infected with three different viruses including Cucumber mosaic virus, Tomato spotted wilt virus, and Potato virus X have been performed using the chrysanthemum 135K microarray. Mock and each virus infected chrysanthemum plants were subjected for microarray analysis.
2015-01-01 | E-GEOD-55985 | biostudies-arrayexpress
Project description:Bactericidal antibiotics are powerful drugs because they not only inhibit essential bacterial functions, but convert them into toxic processes. Many bacteria are remarkably tolerant against antibiotics, due to inducible damage repair responses. How these responses promote whole population tolerance in important human pathogens is poorly understood. The two-component system VxrAB of the diarrheal pathogen Vibrio cholerae, a model system for tolerance against cell wall damaging (e.g., beta-lactam) antibiotics, is required for high-level beta-lactam tolerance. Here, we report the mechanism of VxrAB-mediated survival. We find that -lactam antibiotics inappropriately induce the Fur-regulated iron starvation response, causing an increase in intracellular free iron and colateral oxidative damage. VxrAB reduces antibiotic-induced toxic influx of Fe by downregulating iron importers and induces cell wall synthesis functions to counteract cell wall damage. Our results highlight the complex responses elicited by antibiotics and suggest that the ability to counteract diverse stresses promotes high-level antibiotic tolerance.
2019-07-30 | GSE135010 | GEO
Project description:Bactericidal antibiotics are powerful drugs because they not only inhibit essential bacterial functions, but convert them into toxic processes. Many bacteria are remarkably tolerant against antibiotics, due to inducible damage repair responses. How these responses promote whole population tolerance in important human pathogens is poorly understood. The two-component system VxrAB of the diarrheal pathogen Vibrio cholerae, a model system for tolerance against cell wall damaging (e.g., beta-lactam) antibiotics, is required for high-level beta-lactam tolerance. Here, we report the mechanism of VxrAB-mediated survival. We find that -lactam antibiotics inappropriately induce the Fur-regulated iron starvation response, causing an increase in intracellular free iron and colateral oxidative damage. VxrAB reduces antibiotic-induced toxic influx of Fe by downregulating iron importers and induces cell wall synthesis functions to counteract cell wall damage. Our results highlight the complex responses elicited by antibiotics and suggest that the ability to counteract diverse stresses promotes high-level antibiotic tolerance.
2019-07-30 | GSE135009 | GEO
Project description:Gene expression analysis of chrysanthemum infected with three different viruses including Cucumber mosaic virus, Tomato spotted wilt virus, and Potato virus X have been performed using the chrysanthemum 135K microarray.
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Project description:We generated 12 Gb of high-quality sequencing data (~6 Gb per sample) to clarify the molecular mechanism of salt tolerance between wild tipe and transgenic DgWRKY5 chrysanthemum under normal condition. A total of 1078 differentially expressed genes (DEGs) (593 up-regulated and 485 down-regulated) were identified between CK and DgWRKY5, including genes encoding transcription factors and protein kinases. We identified numerous differentially expressed genes that exhibited distinct expression patterns, and stress-related genes that were highly differentiated in wild tipe and transgenic DgWRKY5 chrysanthemum. These genes have known or potential roles in stress tolerance relative and were enriched in functional gene categories potentially responsible for chrysanthemum resistance. Therefore, they are appealing candidates for further investigation of the gene expression and associated regulatory mechanisms related to stress response .
2018-07-18 | GSE101599 | GEO
Project description:Deeper understanding of antibiotic-induced physiological responses is critical to identifying means for enhancing our current antibiotic arsenal. Bactericidal antibiotics with diverse targets have been hypothesized to kill bacteria, in part, by inducing production of damaging reactive species. This notion has been supported by many groups, but recently challenged. Here we robustly test the hypothesis using biochemical, enzymatic and biophysical assays along with genetic and phenotypic experiments. We first used a novel intracellular hydrogen peroxide (H2O2) sensor, together with a chemically diverse panel of fluorescent dyes sensitive to an array of reactive species, to demonstrate that antibiotics broadly induce redox stress. Subsequent gene expression analyses reveal that complex antibiotic-induced oxidative stress responses are distinct from canonical responses generated by supra-physiological levels of H2O2. We next developed a method to dynamically quantify cellular respiration and found that bactericidal antibiotics elevate oxygen consumption, indicating significant alterations to bacterial redox physiology. We further show that catalase or DNA mismatch repair enzyme overexpression, as well as antioxidant pre-treatment limit antibiotic lethality, indicating that reactive oxygen species causatively contribute to antibiotic killing. Critically, the killing efficacy of antibiotics was diminished under strict anaerobic conditions, but could be enhanced by exposure to molecular oxygen or addition of alternative electron acceptors, suggesting that environmental factors play a role in killing cells physiologically primed for death. This work provides direct evidence that bactericidal antibiotics, downstream of their target-specific interactions, induce complex redox alterations that contribute to cellular damage and death, thus supporting an evolving, expanded model of antibiotic lethality. Here, we used microarrays to analyze oxidative stress responses to bactericidal antibiotic treatment in wildtype and mutant E coli WT or mutant E coli cells were grown to OD ~0.3. Untreated cells were harvested at time 0 as controls. Treated cells given the appropriate chemical perturbation and harvested 1 hour post-treatment. All experiments were performed in technical triplicate.
2014-04-02 | E-GEOD-56133 | biostudies-arrayexpress