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Dysregulation of Streptococcus pneumoniae zinc homeostasis breaks ampicillin resistance in a pneumonia infection model

ABSTRACT: Dysregulation of Streptococcus pneumoniae zinc homeostasis breaks ampicillin resistance in a pneumonia infection model

PROVIDER: PRJNA670849 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12883136.fastq.gz	Fastqsanger.gz
	SRR12883137.fastq.gz	Fastqsanger.gz
	SRR12883138.fastq.gz	Fastqsanger.gz

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Dysregulation of Streptococcus pneumoniae zinc homeostasis breaks ampicillin resistance in a pneumonia infection model

Project description:Streptococcus pneumoniae is the primary cause of community-acquired bacterial pneumonia with rates of penicillin and multi-drug resistance exceeding 80% and 40%, respectively. The innate immune response generates a variety of antimicrobial agents to control infection including zinc stress. Here, we characterized the impact of zinc intoxication on S. pneumoniae, revealing disruptions in central carbon metabolism, lipid biogenesis and peptidoglycan biosynthesis. Characterization of the pivotal peptidoglycan biosynthetic enzyme GlmU revealed an exquisite sensitivity to zinc inhibition. Disruption of the sole zinc efflux pathway, czcD, rendered S. pneumoniae highly susceptible to β-lactam antibiotics. To dysregulate zinc homeostasis in the wild-type strain, we investigated the safe-for-human use ionophore PBT2. PBT2 rendered wild-type S. pneumoniae strains sensitive to a range of antibiotics. Using an invasive ampicillin-resistant strain, we demonstrate in a murine pneumonia infection model the efficacy of PBT2+ampicillin treatment. These findings present a therapeutic modality to break resistance of drug-resistant S. pneumoniae.

2022-02-23 | MTBLS318 | MetaboLights

Dysregulation of Streptococcus pneumoniae zinc homeostasis breaks ampicillin resistance in a pneumonia infection model

Project description:This study reports on the co-administration of a zinc ionophore (PBT-2) and ampicillin to break antibiotic resistance of Streptococcus pneumoniae in a murine pneumonia model. The molecular mechanism for this heightened antimicrobial activity was identified through transcriptomic and metabolomic analyses of a wild type strain and a zinc efflux mutant to identify cellular targets of zinc intoxication. This revealed that zinc intoxication induces numerous cellular disruptions, which when combined with frontline antibiotics, can break antibiotic resistance and potentially preclude further resistance from emerging.

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