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Colistin heteroresistance in Enterobacter cloacae is regualted by PhoPQ-dependent 4-amino-4-deoxy-L arabinose addition to lipid A

ABSTRACT: Colistin heteroresistance in Enterobacter cloacae is regualted by PhoPQ-dependent 4-amino-4-deoxy-L arabinose addition to lipid A

PROVIDER: PRJNA525427 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8665990.fastq.gz	Fastqsanger.gz
	SRR8665991.fastq.gz	Fastqsanger.gz
	SRR8665992.fastq.gz	Fastqsanger.gz

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Colistin heteroresistance in Enterobacter cloacae is regualted by PhoPQ-dependent 4-amino-4-deoxy-L arabinose addition to lipid A

Project description:We report the transcriptional expression from wild type, ΔphoPQ, and ΔpmrAB to understand their contribution to colistin resistance.

2019-06-20 | GSE127802 | GEO

Kp Wt_OXA48 COLISTIN HETERORESISTANCE

Project description:Klebsiella pneumoniae clinical isolates, OXA48 and Wt, colistin heteroresistance

| PRJEB66360 | ENA

Colistin heteroresistance in Enterobacter cloacae is regulated by PhoPQ-dependent 4-amino-4-deoxy-l-arabinose addition to lipid A.

Project description:The Enterobacter cloacae complex (ECC) consists of closely related bacteria commonly associated with the human microbiota. ECC are increasingly isolated from healthcare-associated infections, demonstrating that these Enterobacteriaceae are emerging nosocomial pathogens. ECC can rapidly acquire multidrug resistance to conventional antibiotics. Cationic antimicrobial peptides (CAMPs) have served as therapeutic alternatives because they target the highly conserved lipid A component of the Gram-negative outer membrane. Many Enterobacteriaceae fortify their outer membrane with cationic amine-containing moieties to prevent CAMP binding, which can lead to cell lysis. The PmrAB two-component system (TCS) directly activates 4-amino-4-deoxy-l-arabinose (l-Ara4N) biosynthesis to result in cationic amine moiety addition to lipid A in many Enterobacteriaceae such as E. coli and Salmonella. In contrast, PmrAB is dispensable for CAMP resistance in E. cloacae. Interestingly, some ECC clusters exhibit colistin heteroresistance, where a subpopulation of cells exhibit clinically significant resistance levels compared to the majority population. We demonstrate that E. cloacae lipid A is modified with l-Ara4N to induce CAMP heteroresistance and the regulatory mechanism is independent of the PmrABEcl TCS. Instead, PhoPEcl binds to the arnBEcl promoter to induce l-Ara4N biosynthesis and PmrAB-independent addition to the lipid A disaccharolipid. Therefore, PhoPQEcl contributes to regulation of CAMP heteroresistance in some ECC clusters.

| S-EPMC6561824 | biostudies-literature

Proteomic changes of Klebsiella pneumoniae in response to colistin treatment and crrB mutation-mediated colistin resistance

Project description:Polymyxins are increasingly used as the critical last-resort therapeutic options for multidrug-resistant gram-negative bacteria. Unfortunately, polymyxin resistance has increased gradually for the last few years. Although studies on mechanisms of polymyxin are expanding, system-wide analyses of the underlying mechanism for polymyxin resistance and stress response are still lacking. To understand how Klebsiella pneumoniae adapt to colistin (polymyxin E) pressure, we carried out proteomic analysis of Klebsiella pneumoniae strain cultured with different concentrations of colistin. Our results showed that the proteomic responses to colistin treatment in Klebsiella pneumoniae involving several pathways, including (i) gluconeogenesis and TCA cycle; (ii) arginine biosynthesis; (iii) porphyrin and chlorophyll metabolism; and (iv) enterobactin biosynthesis. Interestingly, decreased abundance of class A β-lactamases including TEM, SHV-11, SHV-4 were observed in cells treated with colistin. Moreover, we also present comprehensive proteome atlases of paired polymyxin-susceptible and -resistant Klebsiella pneumoniae strains. The polymyxin-resistant strain Ci, a mutant of Klebsiella pneumoniae ATCC BAA 2146, showed missense mutation in crrB. The crrB mutant Ci, which displayed lipid A modification with 4-amino-4-deoxy-L-arabinose (L-Ara4N) and palmitoylation, showed striking increases of CrrAB, PmrAB, PhoPQ, ArnBCADT and PagP. We hypothesize that crrB mutations induce elevated expression of the arnBCADTEF operon and pagP via PmrAB and PhoPQ. Moreover, multidrug efflux pump KexD, which was induced by crrB mutation, also contributed to colistin resistance. Overall, our results demonstrated proteomic responses to colistin treatment and the mechanism of CrrB-mediate colistin resistance, which may further offer valuable information to manage polymyxin resistance.

2022-04-11 | PXD018528 | Pride

Colistin resistant A. baumannii: genomic and transcriptomic traits acquired under colistin therapy

Project description:Comparative Genomic and Transcriptomic Characterization of Colistin-Resistant Acinetobacter baumannii

2019-01-23 | GSE109951 | GEO

Aminocandin versus Aminocandin plus Colistin

Project description:We found that the antibiotic colistin acts synergistically with antifungals of the echinocandin class (e.g. aminocandin) on C. albicans cells. In order to elucidate the mode of action of colistin in fungi we performed microarray analysis of samples treated with only aminocandin (0.00125µg/ml) or treated with aminocandin (0.00125µg/ml) and colistin (5µg/ml). We compared: (A). untreated cells to cells treated with aminocandin only; (B). cells treated with aminocandin to cells treated with aminocandin and colistin (which is the focus of this experiment). By comparing those datasets it should be possible to identify genes differentially expressed in response to aminocandin and in response to both drugs. And subsequently to be able to interpret where in the cell colistin acts. (See related experiment in ArrayExpress: E-MEXP-3437 for comparison between untreated cells vs cells treated with aminocandin only.)

2012-03-03 | E-MEXP-3438 | biostudies-arrayexpress

Project description:Colistin heteroresistance

| PRJEB12511 | ENA

Project description:Colistin heteroresistance

| PRJEB12512 | ENA

Colistin dependence in multidrug-resistant Acinetobacter baumannii

Project description:Here we investigated colistin effects on A. baumannii, employing a Mass spectrometry approach and comparing a colistin-susceptible multidrug-resistantclinical isolate to its colistin-dependent subpopulation obtained by subsequent passages in moderate colistin concentrations. Colistin dependence might represent a stepping-stone to resistance, but the mechanisms of colistin dependence are far from clear.

2021-01-12 | PXD020218 | Pride

Transcriptome analysis of arabinose fermentation by engineered Saccharomyces cerevisiae

Project description:Saccharomyces cerevisiae IMS0002 which, after metabolic and evolutionary engineering, ferments the pentose sugar arabinose. Glucose and arabinose-limited anaerobic chemostat cultures of IMS0002 and its non-evolved ancestor IMS0001 were subjected to transcriptome analysis to identify key genetic changes contributing to efficient arabinose utilization by strain IMS0002.

2011-03-01 | GSE27539 | GEO

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