Acinetobacter baumannii VEB
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PROVIDER: PRJNA13000 | ENA |
REPOSITORIES: ENA
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Project description:Acinetobacter baumannii is a major cause of nosocomial infections which can survive in different hospital environments and its multidrug-resistant capacity is major concern now-a-days. ppGpp dependent stringent response mediates reprogramming of gene expression with diverse function in many bacteria. A baumannii A1S_0579 gene is responsible for ppGpp production. Transcriptome analysis of early stationary phase cultures represents several differentially expressed genes in ppGpp deficient strain (∆A1S_0579). We found that the expression of csu operon, which is important in pili biosynthesis for early biofilm formation, was significantly reduced in the ppGpp-deficient strain. Our findings showed that ppGpp signaling plays critical role in biofilm formation, surface motility, adherence and virulence of A baumannii. This study is the first demonstration of the association between ppGpp and pathogenicity of A. baumannii.
2021-05-01 | GSE173627 | GEO
Project description:The increasing rate of antibiotic-resistant bacteria has become a serious health threat. Thus, it is important to discover, characterize, and optimize new molecules to overcome infections caused by these bacteria. It is known that Acinetobacter baumannii has a high capacity to avoid antibacterial drugs. Consequently, these bacteria have emerged as one of responsible for hospital and community-acquired infections. However, how this pathogen infects and survives inside the host cell is unknown. Here we analyze the time-resolved transcriptional profile changes on human epithelial HeLa cells after A. baumannii. Our results show how A.baumannii can survive in host cells and starts replication at 4 hours post infection. We sequenced RNA to obtain a set of differentially expressed gen (DEGs) used for a Gene Ontology (GO) and KEGG pathway analysis. The results show us how host bacteria is altering the host cells environment for their own benefit. We also determine chromosomal regions affected by our set of genes. Furthermore, we obtain protein-protein networks that reveal highly interacted proteins. The combination of these results will pave the way to discover new antimicrobial candidates for multidrug-resistant bacteria.
2021-01-15 | GSE161833 | GEO
Project description:Nosocomial outbreaks of infections caused by multidrug-resistant Acinetobacter baumannii have emerged as a serious threat to human health. The phosphoproteomics of pathogenic bacteria have been investigated for their role in virulence regulation networks. In this study, we analyzed the phosphoproteomics of two clinical isolates of A. baumannii: imipenem-sensitive strain SK17-S and -resistant strain SK17-R.
2015-10-27 | PXD002033 | Pride
Project description:Using Nanopore sequencing, our study has revealed a close correlation between genomic methylation levels and antibiotic resistance rates in Acinetobacter Baumannii. Specifically, the combined genome-wide DNA methylome and transcriptome analysis revealed the first epigenetic-based antibiotic-resistance mechanism in A. baumannii. Our findings suggest that the precise location of methylation sites along the chromosome could provide new diagnostic markers and drug targets to improve the management of multidrug-resistant A. baumannii infections.
2023-09-01 | E-MTAB-13272 | biostudies-arrayexpress
Project description:Cefiderocol (CFDC) is a novel chlorocatechol-substituted siderophore approved to treat complicated urinary tract infections and for hospital-acquired and ventilator-acquired pneumonia. In previous work, human fluids, were shown to increase the minimum inhibitory concentration (MICs) of Acinetobacter baumannii against CFDC and reduce the expression of genes related to iron uptake systems, which could explain the need for higher concentrations of CFDC to exert inhibitory action. Herein, we analyzed the impact of human urine (HU), which contains low albumin concentrations, on the expression of iron-uptake related genes and MIC values of two carbapenem-resistant A. baumannii. Levels of resistance to CFDC were not modified by HU in strain AMA40 but were reduced in the case of strain AB5075. Testing other carbapenem-resistant A. baumannii isolates showed that the CFDC MICs were unmodified or reduced in the presence of HU. The expression of piuA, pirA, bauA, and bfnH determined by qRT-PCR was enhanced in both strains when HU was present in the culture medium. All four tested genes are involved in recognizing ferric siderophore complexes or internalization into the cell’s cytosol. In contrast, the effect of HU on genes associated with resistance to β-lactams, antibiotics commonly used to treat urinary tract infections caused by A. baumannii, was variable; the transcriptional analysis of pbp1, pbp3, blaOXA-51-like, blaADC, and blaNDM-1 showed significant variation. In summary, HU, probably due to the albumin and free iron content, does not adversely impact or slightly improves the activity of CFDC when tested against A. baumannii in urine in contrast to other human bodily fluids.
2022-06-01 | GSE201259 | GEO
Project description:Transcriptomics by RNA-seq provides unparalleled insight into bacterial gene expression networks, enabling a deeper understanding of the regulation of pathogenicity, mechanisms of antimicrobial resistance, metabolism, and other cellular processes. Here we present the transcriptome architecture of Acinetobacter baumannii ATCC 17978, a species emerging as a leading cause of antimicrobial resistant nosocomial infections. Differential RNA-seq (dRNA-seq) examination of model strain ATCC 17978 in 16 laboratory conditions identified 3731 transcriptional start sites (TSS), and 110 small RNAs, including the first identification of 22 sRNA encoded at the 3′ end of mRNA.
2018-06-25 | GSE103244 | GEO
Project description:Background: Acinetobacter baumannii is one of the most dangerous multidrug-resistant pathogens worldwide. Currently, 50-70% of clinical isolates of A. baumannii are extensively drug-resistant (XDR) and available antibiotic options against A. baumannii infections are limited. There are still needs to discover specific de facto bacterial antigenic proteins that could be effective vaccine candidates in human infection. With the growth of research in recent years, several candidate molecules have been identified for vaccine development. So far, there is no public health authorities approved vaccine against A. baumannii. Methods: The purpose of this study was to identify immunodominant vaccine candidate proteins that can be immunoprecipitated specifically with patients’ IgGs. Relaying on hypothesis that IgGs of infected person have capacity to capture immunodominant bacterial proteins. Herein, outer membrane and secreted proteins of sensitive and drug resistant A. baumannii were captured by using IgGs obtained from patient and healthy control sera and were identified by LC-MS/MS analysis. Results: By using subtractive proteomic approach, we determined 34 unique proteins which were captured only in drug-resistant A. baumannii strain via patient sera. After extensive evaluation of predicted epitope regions, solubility, membrane transverse characteristics, and structural properties, we selected several notable vaccine candidates. Conclusion: We identified vaccine candidate proteins that triggered de facto response of human immune system against the antibiotic-resistant A. baumannii. Precipitation of bacterial proteins via patient immunoglobulins was a novel approach to identify the proteins which have potential to trigger to response in patient immune system.
2022-11-02 | PXD037507 | Pride
Project description:Opportunistic pathogen Acinetobacter baumannii possesses stress tolerance strategies against host innate immunity and antibiotic killing. However, how the host-pathogen-antibiotic interaction affects the overall molecular regulation of pro- and anti-pathogenic machineries remains unexplored. Here, we simultaneously investigate proteomic changes in A. baumannii and macrophages following infection in the absence or presence of the last-line polymyxins. We discover that macrophages and polymyxins exhibit complementary effects to disarm several A. baumannii stress tolerance and survival strategies, including oxidative stress resistance, copper tolerance, bacterial iron acquisition and stringent response regulation systems. Using bacterial mutants with impaired stringent response associated (p)ppGpp synthetase/hydrolase spoT we demonstrate that spot mutants exhibit significantly enhanced susceptibility to polymyxin killing and reduced in vivo survivability compared to the wild-type strain. Together, our findings highlight that improved understanding of host-pathogen-antibiotic interplay is critical for optimisation of antibiotic use in patients and discovery of new antibiotics to tackle multidrug-resistant bacterial infections.
2022-02-11 | PXD028502 | Pride
Project description:Acinetobacter baumannii has emerged as one of the most problematic opportunist bacterial pathogen responsible for hospital-acquired and community infections worldwide. Besides its high capacities to acquire antibiotic resistance mechanisms, it also presents high adhesion abilities on inert and living surfaces leading to biofilm development, a lifestyle conferring an additional protection against various treatments, and allowing it to persist for long periods in various hospital niches. Due to their increasing resilience to antimicrobial treatments, A. baumannii biofilms are difficult to control and ultimately eradicate. Overcoming the significant challenges pose by A. baumannii require fundamental insights into mechanisms involved in the development of mature biofilm and thus, may help to develop novel strategies for biofilm prevention and control. To unravel critical determinants of this sessile lifestyle, we compared the proteome profiles of bacteria grown in planktonic stationary phase with those of two A. baumannii strains (ATCC 17978 and SDF), harboring specific features regarding biofilm formation, grown in mature solid-liquid (S-L) biofilm using a proteomic quantitative study. Of interest, among the 69 common proteins determinants accumulated in the two strains at the S-L interface, we sorted out the MacAB-TolC system. This tripartite efflux pump appears to play a role in A. baumannii biofilm formation as demonstrated by using ΔmacAB-tolC deletion mutant. Complementary approaches allowed us to get an overview of the impact of macAB-tolC deletion in A. baumannii physiology. Indeed, this efflux pump appeared to be involved in the envelope stress response occurring in mature biofilm and contributes to maintain WT membrane rigidity as well as tolerance to high osmolarity conditions. In addition, this system is probably involved in the maintenance of iron and sulfur homeostasis. MacAB-TolC might help this pathogen facing and adapting to biofilm architecture which is heterogeneous in space and time, especially in mature biofilm. Increasing our knowledge of A. baumannii biofilm formation will undoubtedly help us develop new therapeutic strategies to tackle this emerging threat to human health.
2022-02-16 | PXD028619 | Pride
Project description:Traditional vaccines are difficult to deploy against the diverse antibiotic-resistant, nosocomial pathogens that cause Hospital Acquired Infections (HAIs). We developed a unique, protein-free vaccine to present antibiotic-resistant HAIs. This vaccine protected mice from invasive infections caused by methicillin-resistant Staphylococcus aureus, vancomycin-resistant Enterococcus faecalis, multidrug resistant Acinetobacter baumannii, Klebsiella pneumoniae, Pseudomonas aeruginosa, Rhizopus delemar, and Candida albicans. Protection persisted even in neutropenic mice infected with A. baumannii or R. delemar. Protection was already apparent after 24 hours and lasted for up to 21 days after a single dose, with a second dose restoring efficacy. Protection persisted without lymphocytes but was abrogated with macrophages depletion. This vaccine induced trained immunity by altering the macrophage epigenetic landscape and the inflammatory response to infection.
2023-08-24 | GSE216061 | GEO