Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1015570 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26053634_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR26053635_subreads.fastq.gz | Fastqsanger.gz |
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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:Klebsiella pneumoniae is an arising threat to human health. However, host immune responses in response to this bacterium remain to be elucidated. The goal of this study was to identify the dominant host immune responses associated with Klebsiella pneumoniae pulmonary infection. Pulmonary mRNA profiles of 6-8-weeks-old BALB/c mice infected with/without Klebsiella pneumoniae were generated by deep sequencing using Illumina Novaseq 6000. qRT–PCR validation was performed using SYBR Green assays. Using KEGG (Kyoto Encyclopedia of Genes and Genomes) analysis, we identified several immune associated pathways, including complement and coagulation cascades, Toll-like receptor signaling pathway, Rap1 signaling pathway, chemokine signaling pathway, TNF signaling pathway, phagosome and NOD-like receptor signaling pathway, were involved in Klebsiella pneumoniae pulmonary infection. Using ICEPOP (Immune CEll POPulation) analysis, we found that several cell types were involved in the host immune response to Klebsiella pneumoniae pulmonary infection, including dendritic cells, macrophages, monocytes, NK (natural killer) cells, stromal cells. Further, IL-17 chemokines were significantly increased during Klebsiella pneumoniae infection. This study provided evidence for further studying the pathogenic mechanism of Klebsiella pneumoniae pneumonia infection.
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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.
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Project description:Hypervirulent Klebsiella pneumoniae ST66-K2 infection
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2012-07-29 | E-GEOD-35822 | biostudies-arrayexpress