Salmonella enterica subsp. enterica
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA478370 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR14512900_1.fastq.gz | Fastqsanger.gz | |||
| SRR14512900_2.fastq.gz | Fastqsanger.gz | |||
| SRR14513000_1.fastq.gz | Fastqsanger.gz | |||
| SRR14513000_2.fastq.gz | Fastqsanger.gz |
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Project description:Long-term effects of antibiotics on Salmonella enterica in feedlot cattle
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Project description:Salmonella enterica causes serious global burden of morbidity and mortality and is a major cause of infant bacteremia in sub Saharan Africa. Diseases caused by Salmonella are treatable with antibiotics but successful antibiotic treatment has become difficult due to antimicrobial resistance. An effective vaccine together with public health effort may therefore be a better strategy to control these infections. Protective immunity against Salmonella depends primarily on T cell-mediated immune responses and therefore identifying relevant T cell antigens is necessary for Salmonella vaccine development. Our laboratory has used an immunoproteomics approach to identify Chlamydia T cell antigens that exhibited significant protection against Chlamydia infection in mice. In this study, we infected murine bone marrow derived dendritic cells from C57BL/6 mice with Salmonella enterica strain SL1344 followed by isolation of MHC class I and II- molecules and elution of bound peptides. The sequences of the peptides were then identified using tandem mass spectrometry. We identified 87 MHC class II and 23 MHC class I Salmonella derived peptides. Four of 12 peptides stimulated IFN-? production by CD4 T cells from the spleens of mice with persistent Salmonella infection. These antigens will be useful for Salmonella immunobiology research and are potential Salmonella vaccine candidates.
2016-12-14 | PXD004451 | Pride
Project description:Cell to cell communication in bacteria to regulate various cellular processes with respect to their population density is termed quorum sensing and is achieved using signaling molecules called autoinducers. LuxS, which is involved in the synthesis of the autoinducer molecule-2 (AI-2), is conserved in several Gram-positive and Gram-negative bacteria including the enteric pathogen Salmonella Typhimurium. Genes that are regulated by luxS in S. Typhimurium were identified using microarrays and RNA samples from wild type S. Typhimurium and its isogenic luxS mutant, in two growth conditions (presence and absence of glucose), and at two different time points (mid-log and early-stationary phases). Minimal differential gene expression was observed in the presence of glucose. In the absence of both luxS and glucose, a total of 1560 genes were differentially expressed and 1361 genes were identified as luxS/AI-2-regulated at the mid-log phase and 199 genes at the early-stationary phase. Quantitative real-time PCR was performed on selected genes to validate the microarray results. These results suggest that although the expression of the luxS gene in S. Typhimurium is independent of the growth condition, its role in the production of AI-2 depends on the growth condition. It was found that luxS/AI-2 plays a vital role in a variety of processes such as metabolism, virulence gene expression, motility, transcription and translation. Keywords: Salmonella Typhimurium, quorum sensing, luxS mutant, autoinducer-2
2009-10-22 | GSE7558 | GEO
Project description:Many non-typhoidal serovars of Salmonella such as Salmonella enterica serovar Typhimurium (S. Typhimurium) are the leading cause of food-borne gastroenteritis, resulting in millions of infections each year and sometimes death. Salmonella enterica serovar Typhimurium is the most common non-typhoidal Salmonella strain isolated from patients around the world and is used as a mouse model to study bacterial pathogenesis and host-microbe interactions. Furthermore, S. Typhimurium is an important pathogen in livestock animals including chickens and cattle. S. Typhimurium utilises a multitude of virulence factors to reach and invade host cells and for its intracellular survival. However, little is known about the mechanism of protein synthesis of these virulence factors at the codon level. Here, we performed RNA-seq and ribosome profiling. Ribosome profiling allows the global mapping of translating ribosomes on the transcriptome and therefore provides direct measure of protein synthesis.
2023-04-01 | E-MTAB-8808 | biostudies-arrayexpress
Project description:Salmonella is an important enteric pathogen that causes a spectrum of diseases varying from mild gastroenteritis to life threatening typhoid fever. Salmonella does not have lac operon. However, E. Coli, Salmonella’s close relative, has lac operon. Being an enteric pathogen like E. coli, Salmonella will also benefit from lac operon. Then, why Salmonella has lost lac operon?. To address this question, lacI, an important component of lac operon was expressed in Salmonella via pTrc99A plasmid. As a control, pTrc99A without lacI was also expressed in Salmonella. The effect of LacI on the transcription profile of Salmonella was analyzed using microarray technique.
2009-05-07 | GSE15950 | GEO
Project description:<p>The gut microbiota is increasingly recognized for playing a critical role in human health and disease, especially in conferring resistance to both virulent pathogens such as Salmonella, which infects 1.2 million people in the United States every year [1], and opportunistic pathogens like Candida, which causes an estimated 46,000 cases of invasive candidiasis each year in the United States [2]. The dynamics of pathogen-microbiome interactions and the metabolites involved in this process remain largely unknown. </p><p>We use gnotobiotic mice infected with the virulent pathogen Salmonella enterica serovar Typhimurium or the opportunistic pathogen Candida albicans in combination with metagenomics and discovery metabolomics to identify changes in the community and metabolome during infection. To isolate the role of the microbiota in response to pathogens, we compared mice monocolonized with the pathogen, uninfected mice 'humanized' with a synthetic human microbiome, or infected humanized mice. We observe that changes in the community and in biosynthetic gene cluster potential occur within 3 days for the virulent Salmonella enterica serovar Typhimurium, but there are minimal changes with a poorly colonizing Candida albicans. In addition, the metabolome shifts depending on infection status, including changes in glutathione metabolites in response to Salmonella infection. The LC-MS metabolomic fingerprint of the cecum differed between mice monocolonized with either pathogen and humanized infected mice. Specifically, we identified an increase in glutathione disulfide, glutathione cysteine disulfide, inosine 5'-monophosphate, and hydroxybutyrylcarnitine in mice infected with Salmonella in contrast to uninfected mice and mice monocolonized with Salmonella. These metabolites potentially play a role in pathogen-induced oxidative stress. These results provide insight into how the microbiota community members interact with each other and with pathogens on a metabolic level.</p><p><br></p><p>Ref:</p><p>[1] Scallan E, Hoekstra RM, Angulo FJ, Tauxe RV, Widdowson MA, Roy SL, Jones JL, and Griffin PM. Foodborne Illness Acquired in the United States—Major Pathogens. Emerg Infect Dis 2011;17:7-15. doi.org/10.3201/eid1701.P11101</p><p>[2] Centers for Disease Control and Prevention, Antibiotic Resistance Threats in the United States, 2013</p>
2019-09-20 | MTBLS753 | MetaboLights
Project description:The nasopharyngeal microbiota of healthy cattle vs. cattle diagnosed with BRD in a commercial feedlot setting was compared using a high-density 16S rRNA microarray (Phylochip). Nasopharyngeal samples were taken from both groups of animals (n=5) at feedlot entry (day 0) and >60 days later.
2015-06-21 | E-MTAB-3430 | biostudies-arrayexpress
Project description:Infection with Salmonella enterica serovar Typhi in humans causes the systemic, life-threatening disease typhoid fever. In the laboratory, typhoid fever can be modeled through the inoculation of susceptible mice with Salmonella enterica serovar Typhimurium. The ensuing disease is characterized by systemic dissemination and colonization of many organs, including the liver, spleen and gallbladder. Using this murine model, we previously characterized the interactions between Salmonella Typhimurium and host cells in the gallbladder and showed that this pathogen can successfully invade gallbladder epithelial cells and proliferate. Additionally, we showed that Salmonella Typhimurium can use bile phospholipids to grow at high rates. These abilities are likely important for quick colonization of the gallbladder during typhoid fever and further pathogen dissemination through fecal shedding. To further characterize the interactions between Salmonella and the gallbladder environment we compared the transcriptome of Salmonella cultures grown in LB or physiological murine bile. Our data showed that many genes involved in bacterial central metabolism are affected by bile, with the citric acid cycle being repressed and alternative respiratory systems being activated. Additionally, our study revealed a new aspect of Salmonella interactions with bile through the identification of phoP as a bile-responsive gene. Repression of phoP expression does not involve PhoPQ sensing of a bile component. Due to its critical role in Salmonella virulence, further studies in this area will likely reveal aspects of the interaction between Salmonella and bile that are relevant to disease.
2011-11-10 | GSE33604 | GEO
Project description:Kaiser2014 - Salmonella persistence after ciprofloxacin treatment
The model describes the bacterial tolerance to antibiotics. Using a mouse model for Salmonella diarrhea, the authors have found that bacterial persistence occurs in the presence of the antibiotic ciprofloxacin because Salmonella can exist in two different states. One, the fast-growing population that spreads in the host's tissues and the other, slow-growing "persister" population that hide out inside dendritic cells of the host's immune system and cannot be attacked by the antibiotics. However, this can be killed by adding agents that directly stimulate the host's immune defense.
This model is described in the article:
Cecum lymph node dendritic cells harbor slow-growing bacteria phenotypically tolerant to antibiotic treatment.
Kaiser P, Regoes RR, Dolowschiak T, Wotzka SY, Lengefeld J, Slack E, Grant AJ, Ackermann M, Hardt WD.
PLoS Biol. 2014 Feb 18;12(2):e1001793.
Abstract:
In vivo, antibiotics are often much less efficient than ex vivo and relapses can occur. The reasons for poor in vivo activity are still not completely understood. We have studied the fluoroquinolone antibiotic ciprofloxacin in an animal model for complicated Salmonellosis. High-dose ciprofloxacin treatment efficiently reduced pathogen loads in feces and most organs. However, the cecum draining lymph node (cLN), the gut tissue, and the spleen retained surviving bacteria. In cLN, approximately 10%-20% of the bacteria remained viable. These phenotypically tolerant bacteria lodged mostly within CD103⁺CX₃CR1⁻CD11c⁺ dendritic cells, remained genetically susceptible to ciprofloxacin, were sufficient to reinitiate infection after the end of the therapy, and displayed an extremely slow growth rate, as shown by mathematical analysis of infections with mixed inocula and segregative plasmid experiments. The slow growth was sufficient to explain recalcitrance to antibiotics treatment. Therefore, slow-growing antibiotic-tolerant bacteria lodged within dendritic cells can explain poor in vivo antibiotic activity and relapse. Administration of LPS or CpG, known elicitors of innate immune defense, reduced the loads of tolerant bacteria. Thus, manipulating innate immunity may augment the in vivo activity of antibiotics.
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2024-09-02 | BIOMD0000000527 | BioModels