scholarly journals Quantitative proteomics analysis of Mycoplasma pneumoniae identifies potential macrolide resistance determinants

AMB Express ◽  
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Shaoli Li ◽  
Guanhua Xue ◽  
Hanqing Zhao ◽  
Yanling Feng ◽  
Chao Yan ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Mycoplasma Pneumoniae ◽  
Quantitative Proteomics ◽  
Molecular Mechanisms ◽  
Resistance Mechanisms ◽  
Community Acquired Pneumonia ◽  
Proteomics Analysis ◽  
Tandem Mass Tag ◽  
Peptide Biosynthesis ◽  
Resistant Strains

AbstractMycoplasma pneumoniae is one of the leading causes of community-acquired pneumonia in children and adolescents. Because of the wide application of macrolides in clinical treatment, macrolide-resistant M. pneumoniae strains have become increasingly common worldwide. However, the molecular mechanisms underlying drug resistance in M. pneumoniae are poorly understood. In the present work, we analyzed the whole proteomes of macrolide-sensitive and macrolide-resistant strains of M. pneumoniae using a tandem mass tag-labeling quantitative proteomic technique, Data are available via ProteomeXchange with identifier PXD022220. In total, 165 differentially expressed proteins were identified, of which 80 were upregulated and 85 were downregulated in the drug-resistant strain compared with the sensitive strain. Functional analysis revealed that these proteins were predominantly involved in protein and peptide biosynthesis processes, the ribosome, and transmembrane transporter activity, which implicates them in the mechanism(s) of resistance of M. pneumoniae to macrolides. Our results provide new insights into drug resistance in M. pneumoniae and identify potential targets for further studies on resistance mechanisms in this bacterium.

scholarly journals Quantitative proteomics analysis of Mycoplasma pneumoniae identifies potential macrolide resistance determinants

2020 ◽  
Author(s):  
shaoli li ◽  
guanhua xue ◽  
hanqing zhao ◽  
yanling feng ◽  
chao yan ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Mycoplasma Pneumoniae ◽  
Quantitative Proteomics ◽  
Molecular Mechanisms ◽  
Resistance Mechanisms ◽  
Community Acquired Pneumonia ◽  
Proteomics Analysis ◽  
Tandem Mass Tag ◽  
Peptide Biosynthesis ◽  
Resistant Strains

Abstract Mycoplasma pneumoniae is one of the leading causes of community-acquired pneumonia in children and adolescents. Because of the wide application of macrolides in clinical treatment, macrolide-resistant M. pneumoniae strains have become increasingly common worldwide. However, the molecular mechanisms underlying drug resistance in M. pneumoniae are poorly understood. In the present work, we analyzed the whole proteomes of macrolide-sensitive and macrolide-resistant strains of M. pneumoniae using a tandem mass tag-labeling quantitative proteomic technique, Data are available via ProteomeXchange with identifier PXD022220. In total, 165 differentially expressed proteins were identified, of which 80 were upregulated and 85 were downregulated in the drug-resistant strain compared with the sensitive strain. Functional analysis revealed that these proteins were predominantly involved in protein and peptide biosynthesis processes, the ribosome, and transmembrane transporter activity, which implicates them in the mechanism(s) of resistance of M. pneumoniae to macrolides. Our results provide new insights into drug resistance in M. pneumoniae and identify potential targets for further studies on resistance mechanisms in this bacterium.

scholarly journals Drug Resistance Mechanisms ofMycoplasma pneumoniaeto Macrolide Antibiotics

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Xijie Liu ◽  
Yue Jiang ◽  
Xiaogeng Chen ◽  
Jing Li ◽  
Dawei Shi ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Resistance Mechanisms ◽  
23S Rrna ◽  
Macrolide Antibiotics ◽  
Rrna Gene ◽  
Site Mutation ◽  
23S Rrna Gene ◽  
Resistant Strains ◽  
Domain V ◽  
The 16S Rrna Gene

Throat swabs from children with suspectedMycoplasma pneumoniae(M. pneumoniae) infection were cultured for the presence ofM. pneumoniaeand its species specificity using the 16S rRNA gene. Seventy-sixM. pneumoniaestrains isolated from 580 swabs showed that 70 were erythromycin resistant with minimum inhibitory concentrations (MIC) around 32–512 mg/L. FiftyM. pneumoniaestrains (46 resistant, 4 sensitive) were tested for sensitivity to tetracycline, ciprofloxacin, and gentamicin. Tetracycline and ciprofloxacin had some effect, and gentamicin had an effect on the majority ofM. pneumoniaestrains. Domains II and V of the 23S rRNA gene and the ribosomal protein L4 and L22 genes, both of which are considered to be associated with macrolide resistance, were sequenced and the sequences were compared with the corresponding sequences in M129 registered with NCBI and the FH strain. The 70 resistant strains all showed a 2063 or 2064 site mutation in domain V of the 23S rRNA but no mutations in domain II. Site mutations of L4 or L22 can be observed in either resistant or sensitive strains, although it is not known whether this is associated with drug resistance.

scholarly journals A systemic study of indoxacarb resistance in Spodoptera litura revealed complex expression profiles and regulatory mechanism

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Li Shi ◽  
Yao Shi ◽  
Ya Zhang ◽  
Xiaolan Liao
Keyword(s):  
Spodoptera Litura ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Expression Profiles ◽  
Resistance Mechanisms ◽  
Differentially Expressed ◽  
Glutathione S Transferase ◽  
Differentially Expressed Mirnas ◽  
Important Pest ◽  
Resistant Strains

Abstract The tobacco cutworm, Spodoptera litura, is an important pest of crop and vegetable plants worldwide, and its resistance to insecticides have quickly developed. However, the resistance mechanisms of this pest are still unclear. In this study, the change in mRNA and miRNA profiles in the susceptible, indoxacarb-resistant and field indoxacarb-resistant strains of S. litura were characterized. Nine hundred and ten co-up-regulated and 737 co-down-regulated genes were identified in the resistant strains. Further analysis showed that 126 co-differentially expressed genes (co-DEGs) (cytochrome P450, carboxy/cholinesterase, glutathione S-transferase, ATP-binding cassette transporter, UDP-glucuronosyl transferase, aminopeptidase N, sialin, serine protease and cuticle protein) may play important roles in indoxacarb resistance in S. litura. In addition, a total of 91 known and 52 novel miRNAs were identified, and 10 miRNAs were co-differentially expressed in the resistant strains of S. litura. Furthermore, 10 co-differentially expressed miRNAs (co-DEmiRNAs) had predicted co-DEGs according to the expected miRNA-mRNA negative regulation pattern and 37 indoxacarb resistance-related co-DEGs were predicted to be the target genes. These results not only broadened our understanding of molecular mechanisms of insecticide resistance by revealing complicated profiles, but also provide important clues for further study on the mechanisms of miRNAs involved in indoxacarb resistance in S. litura.

Tuberculosis: An Update on Pathophysiology, Molecular Mechanisms of Drug Resistance, Newer Anti-TB Drugs, Treatment Regimens and Host-Di-rected Therapies

2020 ◽  
Vol 21 ◽  
Author(s):  
Pobitra Borah ◽  
Pran Kishore Deb ◽  
Katharigatta N. Venugopala ◽  
Nizar A. Al-Shar’i ◽  
Vinayak Singh ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Molecular Mechanisms ◽  
Resistance Mechanisms ◽  
Cellular Functions ◽  
Pathogenic Potential ◽  
Treatment Regimens ◽  
Latent Tb ◽  
Clinical Advances ◽  
Anti Hiv ◽  
Molecular Interventions

Abstract: The human tuberculosis (TB) is primarily caused by Mycobacterium tuberculosis (Mtb) that inhabits inside and amidst immune cells of the host with adapted physiology to regulate interdependent cellular functions with intact pathogenic potential. The complexity of this disease is attributed to various factors such as the reactivation of latent TB form after prolonged persistence, disease progression specifically in immunocompromised patients, advent of multi- and extensively-drug resistant (MDR and XDR) Mtb strains, adverse effects of tailor-made regimens, and drug-drug interactions among anti-TB drugs and anti-HIV therapies. Thus there is a compelling demand for newer anti-TB drugs or regimens to overcome these obstacles. Considerable multifaceted transformations in the current TB methodologies and molecular interventions underpinning host-pathogen interactions and drug resistance mechanisms may assist to overcome the emerging drug re-sistance. Evidently, recent scientific and clinical advances have revolutionised the diagnosis, prevention and treatment of all forms of the disease. This review sheds light on the current understanding of the pathogenesis of TB disease, molecular mechanisms of drug-resistance, progress on the development of novel or repurposed anti-TB drugs and regimens, host-directed therapies, with particular emphasis on underlying knowledge gaps and prospective for futuristic TB control pro-grams.

Abstract 3209: Elucidating drug resistance mechanisms in melanoma with quantitative proteomics.

2013 ◽  
Author(s):  
Elizabeth Remily-Wood ◽  
Kim Paraiso ◽  
Eirik Haarberg ◽  
Y. Ann Chen ◽  
Vito Rebecca ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Quantitative Proteomics ◽  
Resistance Mechanisms

scholarly journals Mechanisms of drug resistance in ovarian cancer

2021 ◽  
Vol 11 (9) ◽  
pp. 362-367
Author(s):  
Klaudia Żak ◽  
Michał Piwoński ◽  
Paweł Stanicki ◽  
Karolina Kalicka ◽  
Justyna Nowaczek
Keyword(s):  
Ovarian Cancer ◽  
Drug Resistance ◽  
Molecular Mechanisms ◽  
Relevant Literature ◽  
Resistance Mechanisms ◽  
Screening Tools ◽  
Advanced Stage ◽  
Gynecological Cancers ◽  
Common Cancer ◽  
Specific Symptoms

Ovarian cancer is the fifth most common cancer affecting women and the most lethal cancer among the gynecological cancers. Because of the lack of specific symptoms and no special screening tools, it is recognised in an advanced stage. In addition, drug resistance in ovarian cancer is so frequent, that genes and cross-talks between some important pathways are still analysed. In this review, the major and recently identified molecular mechanisms of drug resistance, including platinum, taxane, bevacizumab and PARPi resistance mechanisms in ovarian cancer from relevant literature have been investigated.

ERG11 mutations and upregulation in clinical itraconazole-resistant isolates of Candida krusei

2016 ◽  
Vol 62 (11) ◽  
pp. 938-943 ◽  
Author(s):  
Wenli Feng ◽  
Jing Yang ◽  
Yiru Wang ◽  
Jinyu Chen ◽  
Zhiqin Xi ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Molecular Mechanisms ◽  
Synonymous Codon ◽  
Point Mutations ◽  
Pcr Amplification ◽  
Candida Krusei ◽  
Microdilution Method ◽  
Broth Microdilution Method ◽  
Resistant Strains ◽  
Student’S T

To better understand the association between the ERG11 gene and drug resistance in Candida krusei, C. krusei strains were isolated from patients from January 2010 to May 2013. Susceptibility to 5-fluorocytosine (5-FC), amphotericin B (AMB), voriconazole (VRC), fluconazole (FLC), and itraconazole (ITR) were tested by broth microdilution method. Mutations were detected using PCR amplification and gene sequencing. Expression levels of ERG11 were measured by real-time PCR and compared by a 2-tailed Student’s t test between ITR-susceptible strains and ITR-resistant strains. In total, 15 C. krusei strains were obtained, of which 20.00%, 53.33%, and 40.00% were resistant to 5-FC, FLC, and ITR, respectively, whereas all isolates were susceptible to AMB and VRC. Three synonymous codon substitutions were found in ERG11, including T939C, T642C, and A756T. However, T939C was found in both resistant and susceptible C. krusei strains. The expression level of ERG11 was significantly higher in resistant C. krusei strains (1.34 ± 0.08) than in susceptible C. krusei strains (0.94 ± 0.14) (t = 3.74, p < 0.05). Our study demonstrates that point mutations (T642C and A756T) accompanied with the overexpression of ERG11 might be involved in the molecular mechanisms of drug resistance in C. krusei.

scholarly journals Single-Cell RNA Sequencing and Quantitative Proteomics Analysis Elucidate Marker Genes and Molecular Mechanisms in Hypoplastic Left Heart Patients With Heart Failure

2021 ◽  
Vol 9 ◽  
Author(s):  
Li Ma ◽  
Na Zhou ◽  
Rongjun Zou ◽  
Wanting Shi ◽  
Yuanyuan Luo ◽  
...  
Keyword(s):  
Heart Failure ◽  
Quantitative Proteomics ◽  
Molecular Mechanisms ◽  
Marker Genes ◽  
Left Heart ◽  
Hypoplastic Left Heart ◽  
Hub Genes ◽  
Proteomics Analysis ◽  
Patients With Heart Failure ◽  
Single Cell Rna Sequencing

ObjectiveTo probe markers and molecular mechanisms of the hypoplastic left heart (HLH) by single-cell RNA sequencing (scRNA-seq) and quantitative proteomics analysis.MethodsFollowing data preprocessing, scRNA-seq data of pluripotent stem cell (iPSC)-derived cardiomyocytes from one HLH patient and one control were analyzed by the Seurat package in R. Cell clusters were characterized, which was followed by a pseudotime analysis. Markers in the pseudotime analysis were utilized for functional enrichment analysis. Quantitative proteomics analysis was based on peripheral blood samples from HLH patients without heart failure (HLH-NHF), HLH patients with heart failure (HLH-HF), and healthy controls. Hub genes were identified by the intersection of pseudotime markers and differentially expressed proteins (DE-proteins), which were validated in the GSE77798 dataset, RT-qPCR, and western blot.ResultsCardiomyocytes derived from iPSCs were clustered into mesenchymal stem cells, myocardium, and fibroblast cells. Pseudotime analysis revealed their differentiation trajectory. Markers in the three pseudotime clusters were significantly associated with distinct biological processes and pathways. Finally, three hub genes (MMP2, B2M, and COL5A1) were identified, which were highly expressed in the left (LV) and right (RV) ventricles of HLH patients compared with controls. Furthermore, higher expression levels were detected in HLH patients with or without HF than in controls.ConclusionOur findings elucidate marker genes and molecular mechanisms of HLH, deepening the understanding of the pathogenesis of HLH.

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