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Acid-dependent beta-lactam resistance in Klebsiella pneumoniae is mediated by paralogous class B PBPs and the class A PBP, PBP1b

ABSTRACT: Acid-dependent beta-lactam resistance in Klebsiella pneumoniae is mediated by paralogous class B PBPs and the class A PBP, PBP1b

PROVIDER: PRJNA1234613 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32659553_1.fastq.gz	Fastqsanger.gz
	SRR32659553_2.fastq.gz	Fastqsanger.gz
	SRR32659554_1.fastq.gz	Fastqsanger.gz
	SRR32659554_2.fastq.gz	Fastqsanger.gz
	SRR32659555_1.fastq.gz	Fastqsanger.gz

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Acid-dependent beta-lactam resistance in Klebsiella pneumoniae is mediated by paralogous class B PBPs and the class A PBP, PBP1b

Project description:Klebsiella pneumoniae is a leading cause of global deaths due to antibiotic resistance. Of particular concern, is the rapid expansion within K. pneumoniae lineages of resistance to beta-lactams, the most prescribed class of antibiotics. Additionally, the environmental factors that influence pathogen physiology and, subsequently, antibiotic resistance remain poorly understood. Here we demonstrate that physiologically-relevant drops in culture medium pH result in increased antibiotic resistance particularly towards beta-lactams that inhibit cell division. We identified two genes that contribute to acid-dependent beta-lactam resistance, the class A PBP, PBP1b, and the paralogous class B PBP, PBP3PARA. Loss of either gene increases K. pneumoniae susceptibility to beta-lactams at low pH. Our data suggests that functional redundancy among cell wall synthesis enzymes allows for specialization and ensures that cell wall synthesis occurs robustly across a range of pH conditions.

2025-03-17 | GSE291667 | GEO

Beta-lactam resistant isolates

Project description:Beta-lactam resistant isolates Genome sequencing

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A novel strategy to characterize the pattern of β-lactam antibiotic-induced drug resistance in Acinetobacter baumannii.

Project description:Carbapenem-resistant Acinetobacter baumannii (CRAb) is an urgent public health threat, according to the CDC. This pathogen has few treatment options and causes severe nosocomial infections with >50% fatality rate. Although previous studies have examined the proteome of CRAb, there have been no focused analyses of dynamic changes to β-lactamase expression that may occur due to drug exposure. Here, we present our initial proteomic study of variation in β-lactamase expression that occurs in CRAb with different β-lactam antibiotics. Briefly, drug resistance to Ab (ATCC 19606) was induced by the administration of various classes of β-lactam antibiotics, and the cell-free supernatant was isolated, concentrated, separated by SDS-PAGE, digested with trypsin, and identified by label-free LC-MS-based quantitative proteomics. Thirteen proteins were identified and evaluated using a 1789 sequence database of Ab β-lactamases from UniProt, the majority of which were Class C β-lactamases (≥80%). Importantly, different antibiotics, even those of the same class (e.g. penicillin and amoxicillin), induced non-equivalent responses comprising various isoforms of Class C and D serine-β-lactamases, resulting in unique resistomes. These results open the door to a new approach of analyzing and studying the problem of multi-drug resistance in bacteria that rely strongly on β-lactamase expression.

2023-07-20 | PXD042336 | Pride

Discerning strain specific beta-lactam drug resistance of P. aeruginosa

Project description:P. aeruginosa isolates were grown in LB broth media. The bacterial media was then digested after incubation for 24 hours and analyzed to identify bacterial proteins related to beta-lactam drug resistance. Bottom-up proteomics analysis was performed.

2018-11-04 | PXD010588 | Pride

Co-occurrence of aminoglycoside and beta-lactam resistance in E.coli

Project description:Co-occurrence of aminoglycoside and beta-lactam resistance in E.coli

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β-lactam resistance in S. aureus

Project description:Mutations in the gdpP gene are a clinically relevant mechanism for β-lactam resistance in methicillin resistant Staphylococcus aureus lacking mec determinants

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Beta- lactam antibiotics stimulate biofilm formation in non-typeable Haemophilus influenzae by up-regulating carbohydrate metabolism

Project description:Non-typeable Haemophilus influenzae (NTHi) is a common acute otitis media pathogen, with an incidence that is increased by previous antibiotic treatment. NTHi is also an emerging causative agent of other chronic infections in humans, some linked to morbidity, and all of which impose substantial treatment costs. In this study we explore the possibility that antibiotic exposure may stimulate biofilm formation by NTHi bacteria. We discovered that sub-inhibitory concentrations of beta-lactam antibiotic (i.e., amounts that partially inhibit bacterial growth) stimulated the biofilm-forming ability of NTHi strains, an effect that was strain and antibiotic dependent. When exposed to sub-inhibitory concentrations of beta-lactam antibiotics NTHi strains produced tightly packed biofilms with decreased numbers of culturable bacteria but increased biomass. The ratio of protein per unit weight of biofilm decreased as a result of antibiotic exposure. Antibiotic-stimulated biofilms had altered ultrastructure, and genes involved in glycogen production and transporter function were up regulated in response to antibiotic exposure. Down-regulated genes were linked to multiple metabolic processes but not those involved in stress response. Antibiotic-stimulated biofilm bacteria were more resistant to a lethal dose (10M-BM-5g/mL) of cefuroxime. Our results suggest that beta-lactam antibiotic exposure may act as a signaling molecule that promotes transformation into the biofilm phenotype. Loss of viable bacteria, increase in biofilm biomass and decreased protein production coupled with a concomitant up-regulation of genes involved with glycogen production might result in a biofilm of sessile, metabolically inactive bacteria sustained by stored glycogen. These biofilms may protect surviving bacteria from subsequent antibiotic challenges, and act as a reservoir of viable bacteria once antibiotic exposure has ended. 12 samples

2014-06-04 | E-GEOD-58213 | biostudies-arrayexpress

The LysR‐type transcription factor LsrB regulates beta‐lactam resistance in Agrobacterium tumefaciens

Project description:We investigated the role of the LysR-type transcriptional regulator LsrB (Atu2186) from Agrobacterium tumefaciens C58 (alias A. fabrum C58), which regulates the expression of small-regulatory-RNA (sRNA) and several protein-coding genes, such as ampD (atu2113). In our current study we invesigated the role of LsrB in beta-lactam resistance. For this purpose, we constructed a vtlR/lsrB deletion mutant. Total RNA was isolated from this mutant. Sequencing was done on the Illumina NovaSeq 6000 platform. Wild-type samples that derived from the same experiment were published previously (Kraus et al., 2020) (GEO accession: GSE150941). In the vtlR/lsrB mutant around 800 protein coding genes and around 80 sRNA coding genes were downregulated or upregulated at least three-fold (p value ≤ 0.05). Overall, the results demonstrate the huge regulatory effect of LsrB on the transcriptome of A. tumefaciens. Kraus, A., Weskamp, M., Zierles, J., Balzer, M., Busch, R., Eisfeld, J., et al. (2020) Arginine-rich small proteins with a domain of unknown function DUF1127 play a role in phosphate and carbon metabolism of Agrobacterium tumefaciens. J Bacteriol 202: e00309-20.

2023-08-12 | GSE240243 | GEO

The LysR‐type transcription factor LsrB regulates beta‐lactam resistance in Agrobacterium tumefaciens

Project description:The LysR‐type transcription factor LsrB regulates beta‐lactam resistance in Agrobacterium tumefaciens

| PRJNA1003054 | ENA

Beta- lactam antibiotics stimulate biofilm formation in non-typeable Haemophilus influenzae by up-regulating carbohydrate metabolism

Project description:Non-typeable Haemophilus influenzae (NTHi) is a common acute otitis media pathogen, with an incidence that is increased by previous antibiotic treatment. NTHi is also an emerging causative agent of other chronic infections in humans, some linked to morbidity, and all of which impose substantial treatment costs. In this study we explore the possibility that antibiotic exposure may stimulate biofilm formation by NTHi bacteria. We discovered that sub-inhibitory concentrations of beta-lactam antibiotic (i.e., amounts that partially inhibit bacterial growth) stimulated the biofilm-forming ability of NTHi strains, an effect that was strain and antibiotic dependent. When exposed to sub-inhibitory concentrations of beta-lactam antibiotics NTHi strains produced tightly packed biofilms with decreased numbers of culturable bacteria but increased biomass. The ratio of protein per unit weight of biofilm decreased as a result of antibiotic exposure. Antibiotic-stimulated biofilms had altered ultrastructure, and genes involved in glycogen production and transporter function were up regulated in response to antibiotic exposure. Down-regulated genes were linked to multiple metabolic processes but not those involved in stress response. Antibiotic-stimulated biofilm bacteria were more resistant to a lethal dose (10µg/mL) of cefuroxime. Our results suggest that beta-lactam antibiotic exposure may act as a signaling molecule that promotes transformation into the biofilm phenotype. Loss of viable bacteria, increase in biofilm biomass and decreased protein production coupled with a concomitant up-regulation of genes involved with glycogen production might result in a biofilm of sessile, metabolically inactive bacteria sustained by stored glycogen. These biofilms may protect surviving bacteria from subsequent antibiotic challenges, and act as a reservoir of viable bacteria once antibiotic exposure has ended.

2014-06-04 | GSE58213 | GEO

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