Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1270766 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR33783887_1.fastq.gz | Fastqsanger.gz | |||
| SRR33783888_1.fastq.gz | Fastqsanger.gz | |||
| SRR33783889_1.fastq.gz | Fastqsanger.gz | |||
| SRR33783890_1.fastq.gz | Fastqsanger.gz | |||
| SRR33783891_1.fastq.gz | Fastqsanger.gz |
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Project description:Klebsiella pneumoniae is an important human pathogen, causing various infections. Apart from traditional virulence factors, there remains a significant gap in the discovery and research of new chromosomal virulence factors. CpxR is a two-component system (TCS) response regulator, but its impact on the virulence of Klebsiella pneumoniae have not been conclusively determined. For the effect of CpxR on K. pneumoniae virulence, the cpxR deletion(ΔcpxR) strain exhibited reduced serum resistance and attenuated pathogenicity in both Galleria mellonella larvae and mouse infection models compared to the wild-type strain. To identify CpxR-regulated virulence genes, RNA-seq analysis was conducted, followed by deletion of transcription downregulated genes in the ΔcpxR strain. Through serum resistance assays and Galleria mellonella infection experiments, a novel potential virulence factor, KPHS_28080, was identified. Deletion of KPHS_28080 impaired serum survival and proliferation in carbapenem-resistant strains HS11286 and hypervirulent strain ATCC 43816. Furthermore, the ATCC 43816 ΔKPHS_28080 strain showed significantly reduced colonization, proliferation, and multi-organ dissemination capacity in mice, accompanied by diminished pathogenicity. The KPHS_28080 promoter contains a conserved CpxR binding motif, where CpxR binding enhances promoter activity and elevates gene transcription. Sequence alignment revealed that KPHS_28080 is widely conserved across Klebsiella pneumoniae strains, establishing it as a novel chromosome-encoded virulence factor. These results provide a new insight into the CpxR regulation of K. pneumoniae virulence and chromosomal virulence factors.
2025-07-10 | GSE300466 | GEO
Project description:To investigate the role of outer membrane vesicles (OMVs) and related proteins in iron acquisition mechanism of hypervirulent Klebsiella pneumoniae (HVKP) and classic Klebsiella pneumoniae (cKP).
2021-08-21 | PXD028057 |
Project description:Klebsiella pneumoniae is a major pathogen that causes a variety of human infections, posing a significant public health threat. Understanding its pathogenesis is essential for devising effective treatment strategies. In this study, we aim to identify critical virulence factors in K. pneumoniae through analyzing virulence-associated genes that were identified in three transposon mutagenesis libraries. Two genes, wzi and kvrB, are consistently detected across these libraries, indicating their potential as critical virulence factors. While Wzi has usually been implicated in virulence through CPS, its actual function in K. pneumoniae pathogenicity has rarely been explored. Wzi deficiency reduces CPS production in K. pneumoniae, contrasting with its effect in Escherichia coli. Importantly, Wzi exerts a pivotal role in K. pneumoniae pathogenicity in vitro and in vivo, functioning through both CPS-dependent and -independent pathways. Wzi inhibits the secretion of IFN-γ-related cytokines at early infection stage to promote K. pneumoniae survival in the host. Wzi triggers sustained neutrophil recruitment during infection through the upregulation of CXCL1 expression, resulting in the pulmonary barrier damage and increased K. pneumoniae invasion into the bloodstream. Concurrently, Wzi confers K. pneumoniae to counteract neutrophil-mediated clearance in a CPS-dependent manner. Sequence polymorphisms of wzi significantly affect bacterial resistance to serum killing, with alleles frequently associated with hypervirulent K. pneumoniae exhibiting the highest resistance. Collectively, our findings highlight that the dual role of Wzi as a CPS-dependent and -independent virulence factor that combats host clearance during K. pneumoniae infection, representing a promising target for the development of anti-infective treatment against the bug.
2025-02-25 | GSE286873 | GEO
Project description:To investigate the whole-genome gene expression difference between the wild-type and capsule deletion mutant in Klebsiella pneumoniae MGH 78578. The mutants analyzed in this study are further described in Huang T.W., Stapleton J.C., Chang H.Y., Tsai S.F., Palsson B.O., Charusanti P. Capsule removal via lambda-Red knockout system perturbs biofilm formation and fimbriae extression in Klesiella pneumoniae MGH 78578 (manuscript submission) A six chip study using total RNA recovered from three separate wild-type cultures and three separate cultures of a capsule deltion mutant of Klebsiella pneumoniae MGH 78578. The capsule gene cluster (KPN_02493 to KPN_02515) was entirely removed in the capsule deletion mutant. Each chip measures the expression level of 5,305 genes from Klebsiella pneumoniae MGH 78578 and the associated five plasmids (pKPN3, pKPN4, pKPN5, pKPN6 and pKPN7) with 50-mer oligo tiling array with 30-mer spacer.
2013-12-31 | E-GEOD-40011 | biostudies-arrayexpress
Project description:Hypervirulent Klebsiella pneumoniae (HvKP) is an emerging human pathogen causing invasive infection in immune-competent hosts. The hypervirulence is strongly linked to the overproduction of hypermucovisous capsule, but the underlining regulatory mechanism of hypermucoviscosity (HMV) has been elusive, especially at the post-transcriptional level mediated by small RNAs (sRNAs). Using a recently developed RNA interactome profiling approach, we have investigated the Hfq-associated sRNA regulatory network and established the first in vivo RNA-RNA interactome in HvKP. Our data reveal numerous interactions between sRNAs and HMV-related mRNAs, and identify a plethora of sRNA that inhibit or promote HMV. One of the strongest repressors of HMV was ArcZ, a conserved sRNA in the Enterobacteriaceae family. We found that ArcZ is activated by the master regulator of catabolite repression Crp, and down-regulates the expression of mlaA encoding an outer-membrane lipoprotein, leading to decreased HMV and virulence attenuation in mice. ArcZ significantly reduced HMV in several carbapenem-resistant and hypervirulent clinical isolates with diverse genetic background, suggesting it is an antisense RNA inhibitor of HMV with therapeutic potential. In summary, our work provides a comprehensive map of the RNA-RNA interaction network of HvKP and identifies ArcZ as a conserved repressor of HMV, providing novel insights into the mechanisms of posttranscriptional regulations of virulence.
2024-07-17 | GSE260738 | GEO
Project description:The emergence of hypervirulent Klebsiella pneumoniae (hvKP) strains poses a significant threat to public health due to their high mortality rates and propensity to cause severe community-acquired infections in otherwise healthy individuals. The ability of hvKP to form biofilms and produce a protective capsule contributes to its enhanced virulence and is a significant challenge to effective antibiotic treatment. Therefore, understanding the molecular mechanisms underlying hvKP virulence and biofilm formation is crucial for developing new therapeutic strategies. Polyphosphate Kinase 1 (PPK1) is an enzyme responsible for inorganic polyphosphate synthesis and plays a vital role in regulating various physiological processes in bacteria. In this study, we investigated the impact of polyP metabolism on the biofilm and capsule formation and virulence traits in hvKP using Dictyostelium discoideum amoeba as a model host. We found that the PPK1 null-mutant was impaired in biofilm and capsule formation and showed attenuated virulence in D. discoideum compared to the wild-type strain. We performed a shotgun proteomic analysis of the PPK1 mutant and wild-type strain to gain further insight into the underlying molecular mechanism. The results revealed that the PPK1 mutant had a differential expression of proteins (DEP) involved in capsule synthesis (Wzi - Ugd), biofilm formation (MrkC-D-H), synthesis of the colibactin genotoxin precursor (ClbB), as well as proteins associated with the synthesis and modification of lipid A (ArnB -LpxC - PagP). These proteomic findings corroborate the phenotypic observations and indicate that the PPK1 mutation is associated with impaired biofilm and capsule formation and attenuated virulence in hypervirulent K. pneumoniae. Overall, our study highlights the importance of polyP synthesis in regulating extracellular biomolecules and virulence in K. pneumoniae and provides insights into potential therapeutic targets for treating K. pneumoniae infections.
2024-08-23 | PXD046644 | Pride
Project description:Antibiotic use can lead to expansion of multi-drug resistant pathobionts within the gut microbiome that can cause life-threatening infections. Selective alternatives to conventional antibiotics are in dire need. Here, we describe a Klebsiella PhageBank that enables the rapid design of antimicrobial bacteriophage cocktails to treat multi-drug resistant Klebsiella pneumoniae. Using a transposon library in carbapenem-resistant K. pneumoniae, we identified host factors required for phage infection in major Klebsiella phage families. Leveraging the diversity of the PhageBank and experimental evolution strategies, we formulated combinations of phages that minimize the occurrence of phage resistance in vitro. Optimized bacteriophage cocktails selectively suppressed the burden of multi-drug resistant K. pneumoniae in the mouse gut microbiome and drove bacterial populations to lose key virulence factors that act as phage receptors. Further, phage-mediated diversification of bacterial populations in the gut enabled co-evolution of phage variants with higher virulence and a broader host range. Altogether, the Klebsiella PhageBank represents a roadmap for both phage researchers and clinicians to enable phage therapy against a critical multidrug-resistant human pathogen.
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Project description:Hypervirulent Klebsiella pneumoniae (hvKp) is a significant pathogen causing severe community-acquired infections, characterized by the presence of a virulence plasmid. The plasmid-encoded regulator of mucoid phenotype A (RmpA) activates the expression of capsule genes, resulting in a hypermucoviscosity phenotype strongly associated with increased virulence. RmpA features a LuxR DNA-binding domain and a signaling-responsive domain, typical of proteins that regulate multiple biological processes. However, the comprehensive regulatory mechanisms of RmpA in hvKp remain unclear. Herein, RNA-seq showed that RmpA activates carbohydrate metabolism pathways while repressing those related to DNA replication, ribosome metabolism, and biofilm formation. ChIP-seq further confirmed RmpA’s role as a global regulator that not only enhances capsule production by activating transcripts within the capsule locus, but also upregulates the expression of key genes involved in synthesizing capsule precursors. RmpA regulates the phenotypic switch between hypermucoviscosity and biofilm formation by repressing type III fimbriae genes. In addition, Expression of RmpA in Escherichia coli induced global transcriptional changes, suggesting it functions as a global regulator across species. These findings position RmpA as a central regulator in hvKp, orchestrating metabolic pathways and phenotypic traits essential for virulence.
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Project description:Investigation of whole genome gene expression level in Klebsiella pneumoniae MGH78578 grown up to mid-exponential phase in M9 minimal media supplemented with 0.2% glucose A two chip study using total RNA recovered from MGH78578 grown up to OD600nm 0.5 (mid-exponential phase) in M9 minimal media supplemented with 0.2% glucose. The high-density oligonucleotide tiling arrays used were consisted of 392,778 oligonucleotide probes spaced 30 bp apart (20-bp overlap between two probes) across the K. pneumoniae main genome and plasmids.
2012-07-29 | E-GEOD-35746 | biostudies-arrayexpress