Kpneumo 1
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB52868 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| ERR10100601_1.fastq.gz | Fastqsanger.gz | |||
| ERR10100601_2.fastq.gz | Fastqsanger.gz | |||
| ERR10100602_1.fastq.gz | Fastqsanger.gz | |||
| ERR10100602_2.fastq.gz | Fastqsanger.gz |
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Project description:The mammalian gastrointestinal tract harbors a diverse microbiota residing in intimate contact with the host immune system. Though most associations are symbiotic or commensal, some resident bacteria (termed pathobionts) have the potential to induce disease in immunocompromised hosts. Type VI secretion systems (T6SSs) have recently emerged as a novel mechanism for forging microbial-host interactions during infection. We reveal here a unique protective role for the T6SS of Helicobacter hepaticus, a Gram-negative bacterium of the murine intestinal microbiota. The T6SS of H. hepaticus targets effector substrates to intestinal epithelial cells (IECs). Mutants in T6SSs display higher intracellular and cell-associated numbers upon incubation with IECs, and exhibit increased bacterial colonization of the gastrointestinal tract compared to wild-type bacteria. The T6SS accordingly directs an anti-inflammatory gene expression profile in IECs co-cultured with H. hepaticus. Remarkably, T6SS mutants induce an exacerbated pro-inflammatory response in an experimental model of colitis. CD4+ T cells isolated from T6SS mutant-colonized animals produce increased T-helper 17 (Th17) cytokines in response to IECs presenting H. hepaticus antigens. These data demonstrate that H. hepaticus intimately interacts with IECs and employs type VI secretion to establish a balanced host relationship by limiting microbial colonization and intestinal inflammation. We propose that altering host-bacterial equilibriums that lead to dysbiosis of the microbiota contributes to human disorders such as inflammatory bowel disease and colon cancer.
2010-06-01 | GSE20434 | GEO
Project description:TraDIS study to identify novel immunity proteins and their effector proteins associated with the Type VI secretion system (T6SS) in Pseudomonas aeruginosaThese data are part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/
2015-05-12 | E-ERAD-317 | biostudies-arrayexpress
Project description:Metabolites generated in response to infection have a major role in shaping the nature of the immune response. We predicted that the metabolic response to the highly prevalent Klebsiella pneumoniae sequence type 258 (Kp ST258) strains is responsible for their ability to persist in the lungs, despite the expected proinflammatory signaling evoked by LPS. By combining in situ metabolic imaging and comprehensive transcriptional analyses, we demonstrate that Kp ST258 activates host glutaminolysis and fatty acid oxidation (FAO), generating an oxidant-rich microenvironment predisposed to the accumulation of anti-inflammatory monocyte populations. In a setting not unlike that generated by some tumors, metabolically active Kp ST258 elicits an immunotolerant, instead of a proinflammatory response. The bacteria in turn adapt to airway oxidants by upregulation of the Type VI Secretion System (T6SS), which is highly conserved across these strains worldwide. The global success of Kp ST258 can be explained, to a major extent, by their metabolic activity that promotes a permissive immune response to which the bacteria adapt.
2022-08-09 | GSE184563 | GEO
Project description:Metabolites generated in response to infection have a major role in shaping the nature of the immune response. We predicted that the metabolic response to the highly prevalent Klebsiella pneumoniae sequence type 258 (Kp ST258) strains is responsible for their ability to persist in the lungs, despite the expected proinflammatory signaling evoked by LPS. By combining in situ metabolic imaging and comprehensive transcriptional analyses, we demonstrate that Kp ST258 activates host glutaminolysis and fatty acid oxidation (FAO), generating an oxidant-rich microenvironment predisposed to the accumulation of anti-inflammatory monocyte populations. In a setting not unlike that generated by some tumors, metabolically active Kp ST258 elicits an immunotolerant, instead of a proinflammatory response. The bacteria in turn adapt to airway oxidants by upregulation of the Type VI Secretion System (T6SS), which is highly conserved across these strains worldwide. The global success of Kp ST258 can be explained, to a major extent, by their metabolic activity that promotes a permissive immune response to which the bacteria adapt.
2022-08-09 | GSE190262 | GEO
Project description:We report the transcriptome of Burkholderia pseudomallei type VI secretion regulator TctR mutant grown in rich media compared to wild type. The RNA-seq studies confirmed the role of TctR as a negative regulator of T6SS-2, a positive regulator of T6SS-6 and suggest a potential role in regulation of the T6SS-3 and T6SS-4 gene clusters.
2017-10-09 | GSE104716 | GEO
Project description:In order to identify secreted proteins associated with the type VI secretion system (T6SS), the secretome of a wild-type A. baumannii AB307 0294 T6SS active strain was compared to the secretome of a T6SS inactive mutant strain, A. baumannii AB307-0294ΔtssM.
2018-05-25 | PXD009528 | Pride
Project description:To determine whether the Vibrio cholerae type VI secretion system (T6SS) is functional during animal infection, derivatives of V52 were used to infect infant mice. In this infection model, a diarrheal response occurred and effector translocation could be detected. These host responses were dependent on a functional T6SS and on the actin cross-linking effector domain of VgrG-1. Gene expression and histological studies showed innate immune activation and immune cell infiltration in the intestinal lumen.
2010-01-20 | GSE19946 | GEO
Project description:Opportunistic bacterial pathogens require effective mechanisms to compete with other bacteria and to switch between host and environment-adapted states. The Type VI secretion system (T6SS) occurs widely in Gram-negative bacteria and mediates efficient killing of neighbouring competitors. Here we describe the distribution of T6SSs across the genus Serratia and report the unexpected discovery that a highly-conserved antibacterial T6SS is differentially active between closely-related clinical isolates of Serratia marcescens. By combining genomic and experimental approaches, we identified a genus-core two-component system which controls T6SS activity and is subject to very frequent inactivating mutations, exclusively in clinically-derived isolates of S. marcescens. This regulatory system controls a number of lifestyle-related traits at transcriptional and post-translational levels, including T6SS activity, antibiotic production, motility and adhesion. Our data support a model whereby this system represents a conserved, modular switch from sessile to pioneering and aggressive behaviour, which is subject to strong selection pressure in the clinical environment.
2025-01-29 | GSE273522 | GEO
Project description:<p>BolA has been characterized as an important transcriptional regulator, which is induced in the stationary phase of growth and is often associated with bacterial virulence. This study was initiated to elucidate the role of the BolA in the virulence of <em>K. pneumoniae</em>. Using a mouse infection model, we revealed bolA mutant strain yielded significantly decreased bacterial loads in liver, spleen, lung and kidney, and failed to form liver abscesses. Gene deletion demonstrated that the bolA is required for siderophore production, biofilm formation and adhesion to human colon cancer epithelial cells HCT116. Quantitative reverse transcriptase PCR (RT-qPCR) indicated that BolA is able to impact the expression of pulK, pulF, pulE, clpV, vgrG, entE, relA and spoT genes on a genome-wide scale, which are related to type II secretion system (T2SS), type VI secretion system (T6SS), guanosine tetraphosphate (ppGpp) and siderophore synthesis and contributes to fitness in the host. Furthermore, the metabolome analysis showed that the deletion of the bolA gene led to decreased pools of 5 metabolites: biotin, spermine, cadaverine, guanosine and flavin adenine dinucleotide, all of which are involved in pathways related to virulence and stress resistance. Taken together, we provided evidence that BolA is a significant virulence factor in the ability of <em>K. pneumoniae</em> to survive and this is an important step in progress to an understanding of the pathways underlying bacterial virulence.</p>
2022-09-13 | MTBLS2712 | MetaboLights
Project description:We recently demonstrated that colistin resistance in Acinetobacter baumannii can result from mutational inactivation of genes essential for lipid A biosynthesis. Consequently, strains harboring these mutations are unable to produce the major Gram negative bacterial surface component, lipopolysaccharide (LPS). To understand how A. baumannii compensates for the lack of LPS, we compared the transcriptional profile of the A. baumannii type strain ATCC19606, to that of an isogenic, LPS-deficient, lpxA mutant strain. Analysis of the expression profiles indicated that the LPS-deficient strain showed increased expression of many genes involved in cell envelope and membrane biogenesis. In particular, up-regulated genes included those involved in the Lol lipoprotein transport system and the Mla-retrograde phospholipid transport system. In addition, genes involved in the synthesis and transport of poly-beta-1,6-N-acetylglucosamine (PNAG) were also up-regulated and a corresponding increase in PNAG production was observed. The LPS-deficient strain also exhibited reduced expression of genes predicted to encode the fimbrial subunit FimA and a type VI secretion system (T6SS). The reduced expression of genes involved in T6SS correlated with the detection of the T6SS-effector protein, AssC, in culture supernatants of the A. baumannii wild-type strain, but not in the LPS-deficient strain. Taken together, these data show that, in response to total LPS loss, A. baumannii alters the expression of critical transport and biosynthesis systems associated with modulating the composition and structure of the bacterial surface. Comparison of a gene expression in biological duplicate samples derived from parent bacterial strain to an isogenic mutant strain.
2011-08-11 | E-GEOD-31206 | biostudies-arrayexpress