Ontology highlight
ABSTRACT:
PROVIDER: PRJNA648641 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12322183.fastq.gz | Fastqsanger.gz |
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Project description:Tigecycline, a protein translation inhibitor, is a treatment of last resort for infections caused by the opportunistic multidrug resistant human pathogen Acinetobacter baumannii. However, strains resistant to tigecycline were reported not long after its clinical introduction. Translation inhibitor antibiotics perturb ribosome function and induce the reduction of (p)ppGpp, an alarmone involved in the stringent response that negatively modulates ribosome production. Through RNA sequencing, this study revealed a significant reduction in the transcription of genes in citric acid cycle and cell respiration, suggesting tigecycline inhibits or slows down bacterial growth. Our results indicated that the drug-induced reduction of (p)ppGpp level promoted the production but diminished the degradation of ribosomes, which mitigates the translational inhibition effect by tigecycline. The reduction of (p)ppGpp also led to a decrease of transcription coupled nucleotide excision repair which likely increases the chances of development of tigecycline resistant mutants. Increased expression of genes linked to horizontal gene transfer were also observed. The most upregulated gene, rtcB, involving in RNA repair, is either a direct tigecycline stress response or is in response to the transcription de-repression of a toxin-antitoxin system. The most down-regulated genes encode two b-lactamases, which is a possible by-product of tigecycline-induced reduction in transcription of genes associated with peptidoglycan biogenesis. This transcriptomics study provides a global genetic view of why A. baumannii is able to rapidly develop tigecycline resistance.
2020-08-03 | GSE131451 | GEO
Project description:Tigecycline is a broad-spectrum active intravenous antibiotic that is also active against methicillin-resistant staphylococcus aureus. In Phase 3 and 4 clinical trials, increased all-cause mortality was observed in patients treated with tigecycline compared to patients in the control group. The reason for the increase is not yet clear. In this study, we found tigecycline could cause abnormal coagulation in tumor patients, especially in patients with hematological malignancies. The main manifestations were decreased fibrinogen and prolonged activated prothrombin time (APTT), thrombin time (TT) and D-dimer. In addition, functional studies have found that tigecycline could inhibit platelet adhesion and aggregation, and the patient's coagulation function could gradually recover after discontinuation. Gene sequencing results suggested that tigecycline could significantly regulate the expression of genes related to platelet function pathways, and could increase the incidence of single nucleotide polymorphisms and the number of alternative splices in CHO cells with tigecycline treatment. Abnormal platelet function and low numbers are common in patients with hematological malignancies. Our study could explain the mechanism of abnormal coagulation caused by tigecycline. At the same time, a warning should be given when doctors applied tigecycline to cure infections in tumor patients.
2022-06-01 | GSE198830 | GEO
Project description:tigecycline-resistant Acinetobacter baumannii
| PRJNA949386 | ENA
Project description:Proteome of klebsiella pneumoniae KP124andKP126, KP124 is sensitive to tigecycline, KP126 is resistant to tigecycline.
2025-07-24 | PXD066522 |