Klebsiella pneumoniae Expressing VIM-1 Metallo-β-Lactamase Is Resensitized to Cefotaxime via Thiol-Mediated Zinc Chelation

Káradóttir, Harpa; Coorens, Maarten; Liu, Zhihai; Wang, Yang; Agerberth, Birgitta; Giske, Christian G.; Bergman, Peter

doi:10.1128/iai.00756-19

Cited by 7 publications

(5 citation statements)

References 26 publications

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“…However, in recent years, the resistance to piperacillin/tazobactam, cefoperazone/sulbactam, and ampicillin/sulbactam in our hospital has been positively correlated with the use of β -lactams, and the elevated resistance may be attributed to their frequent use. The resistance to ceftazidime was positively correlated with the usage of glycopeptides and carbapenem, which was consistent with the results of previous research [ 21 ], and the high usage of antimicrobial drugs was one of the important causes of Klebsiella pneumonia resistance (all P < 0.05).…”

Section: Discussionsupporting

confidence: 91%

Correlation between Drug Resistance of Klebsiella Pneumonia and Antimicrobial Drug Usage

Liu

Dai

Shen

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Objective. To assess the correlation between the drug resistance of Klebsiella pneumoniae and antimicrobial drug usage. Methods. The drug resistance rate of Klebsiella pneumoniae and the antimicrobial drug dosage of inpatients admitted to The Second Affiliated Hospital of Wannan Medical College from January 2016 to December 2020 were retrospectively recorded, and their correlation was analyzed using the Pearson method. Results. There are 6493 strains of Gram-negative bacteria, including 1272 strains of Klebsiella pneumoniae, ranking first in respiratory medicine. Klebsiella pneumoniae showed an overall increasing trend in resistance to piperacillin/tazobactam and ampicillin/sulbactam and a high resistance to aztreonam, ceftazidime, and ciprofloxacin (all P < 0.05 ). The top 3 antimicrobial drugs used in 2016–2020 were β-lactams, quinolones, and macrolides. The rates of resistance to piperacillin/tazobactam, cefoperazone/sulbactam, and ampicillin/sulbactam were highly positively correlated with the use of β-lactams. The use of carbapenems and glycopeptides was negatively correlated with the resistance to ciprofloxacin, and the resistance to ceftazidime had a high positive correlation with the use of glycopeptides and carbapenems. Conclusion. The use of antimicrobial drugs is correlated with the resistance rate of Klebsiella pneumoniae. To reduce bacterial drug resistance, the rational use of antimicrobial drugs requires joint control through multiple departments to improve the clinical use of antimicrobial drugs and improve in-hospital control.

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Section: Discussionsupporting

confidence: 91%

Correlation between Drug Resistance of Klebsiella Pneumonia and Antimicrobial Drug Usage

Liu

Dai

Shen

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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“…On other hands the MIC of free solution for Escherichia coli is 0.5 µg/ml. The MICs for aqueous cefotaxime sodium agreed with published values [38][39][40][41][42].…”

Section: In Vitro Evaluation Of the Antibacterial Activity Of Cefotax...supporting

confidence: 84%

Cefotaxime Eluting Niosomes as A Novel Approach to Potentiate the Antibacterial Activity

Alhazza¹,

Al-Lami²,

AlShaheen³

et al. 2022

Journal of Pharmaceutical Negative Results

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Multidrug resistance has resulted in hurtful infections on treatment with common antimicrobials and is associated with health threatening problems. Antibiotic abuse in health care systems contributes to global resistance. β-lactams are the predominantly used antibiotics, and the most often used is cefotaxime, therefore facing a resistance problem. Potent cephalosporin derivatives, β-lactamase inhibitors, prodrugs, and drug nano-carriers are approaches to cutback bacterial resistance. An example of a nanocarrier applied in field of antibacterial activity enhancement is niosomes. Niosomes are self-assembled vesicles made from non-ionic surfactants with cholesterol also additives included or omitted that can provide good features such as antibiotic shielding, cleavage proofing, controlled release, and specific targeting. Cefotaxime niosomes preparation done by Thin-Film Hydration method using Tween 40, span 60, stearylamine, and cholesterol. The dried film was moisturised with buffered solution of cefotaxime at 45-55°C then the final nanosized niosomal cefotaxime was generated through a probe sonication. A 27 formulas were prepared and identified by dynamic light scattering so that polydispersity index and the vesicular size are measured. The selected formula of cefotaxime niosomes (CN6) has as showed the lowermost values and a prominent vesicular structure of 106 nm diameter on Transmission electron microscope and compatibility on Fourier Transform Infrared System analysis. CN6 remained unchanged in diameter and Poly-dispersity index after 100 days of storage at 2 to-80 C and also onsubsequent freeze drying and reconstitution. Entrapment efficiency was quantified by the ultracentrifugation method and was discovered to be 93 %. Antibiotic delivery by cefotaxime-eluting niosomes has been shown to be successful with antibacterial potentiation of 160, 8, 640 and 40 times better than aqueous solution against Staphylococcus aureus, Escherichia coli, Klebsiella pneumoniae, and Pseudomonas aeruginosa respectively which is obviously a considerable drop in the minimum inhibitory concentrations of the selected formula versus the aqueous cefotaxime solution and this was evaluated using Agar well diffusion technique.

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“…These results suggest that when system x c − is impaired, keratinocytes can utilize the transsulfuration pathway to generate cysteine; however, cysteine de ciency and related cell death cannot be prevented by promoting only the last step of the transsulfuration pathway. Besides, previous studies claimed that cysteine is an endogenous metal ion chelator [50,51]. Therefore, NAC not only maintains the antioxidant system by providing su cient sulfhydryl, but also can chelate ZnO NPs or Zn 2+ to alleviate ZnO NP-induced cell damage.…”

Section: Discussionmentioning

confidence: 99%

ZnO NPs delay the recovery of psoriasis-like skin lesions through promoting inflammation and keratinocyte apoptosis via nuclear translocation of phosphorylated NF-κB p65 and cysteine deficiency

Lai

Wang

Zhu

et al. 2020

Preprint

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Background This study aimed to confirm the safety and risk of applying zinc oxide nanoparticles (ZnO NPs) to pathological skin, such as psoriasis-like skin. The majority of previous studies confirmed the safety of applying ZnO NPs to normal skin. However, we know very little about the risks of using sunscreen, cosmetics and topical drugs containing ZnO NPs for individuals with skin diseases. In addition, some studies claimed that ZnO NPs can penetrate normal or pathological skin, and ZnO NPs have frequently been reported to have proinflammatory and lethal effects in vitro. Therefore, it is necessary to evaluate the safety of applying ZnO NPs to pathological skin. Results ZnO NPs passed through gaps between keratinocytes and entered stratum basale of epidermis and dermis in imiquimod (IMQ)-induced psoriasis-like skin lesions. Application of a ZnO NP-containing suspension for 3 connective days delayed the healing of the epidermal barrier; increased the expression levels of inflammatory cytokines; promoted keratinocyte apoptosis and disturbed redox homeostasis. In vitro, ZnO NPs promoted TNF-α, IL-1β and IL-6 secretion and apoptosis of recombinant-human-TNF-α-stimulated HaCaT cells. NF-κB, ERK, p38 and JNK inhibitors blocked ZnO NP-induced inflammation. JSH-23, an inhibitor of the nuclear translocation of p-NF-κB p65, and NAC, an acetylated precursor of L-cysteine, not only inhibited the ZnO NP-induced inflammation but also inhibited apoptosis and cysteine deficiency. Neither erastin nor RSL3 induced p-NF-κB p65 nuclear translocation, but they did reduce cysteine biosynthesis. Additionally, ferropstatin-1, an inhibitor of lipid peroxidation, partially rescued ZnO NP-induced decreases in cell viability and cysteine content. Conclusions ZnO NPs delay the recovery of psoriasis-like skin lesions through promoting inflammation and keratinocyte apoptosis via the nuclear translocation of phosphorylated NF-κB p65 and cysteine deficiency. This work reminds the public that ZnO NPs are not safe for pathological skin, especially in inflammatory skin diseases such as psoriasis, and has revealed a partial mechanism by which ZnO NPs delay the recovery of pathological skin, promoting the appropriate use of ZnO NPs.

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Klebsiella pneumoniae Expressing VIM-1 Metallo-β-Lactamase Is Resensitized to Cefotaxime via Thiol-Mediated Zinc Chelation

Cited by 7 publications

References 26 publications

Correlation between Drug Resistance of Klebsiella Pneumonia and Antimicrobial Drug Usage

Correlation between Drug Resistance of Klebsiella Pneumonia and Antimicrobial Drug Usage

Cefotaxime Eluting Niosomes as A Novel Approach to Potentiate the Antibacterial Activity

ZnO NPs delay the recovery of psoriasis-like skin lesions through promoting inflammation and keratinocyte apoptosis via nuclear translocation of phosphorylated NF-κB p65 and cysteine deficiency

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