Ontology highlight
ABSTRACT:
PROVIDER: PRJNA861796 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20610760_1.fastq.gz | Fastqsanger.gz | |||
| SRR20610760_2.fastq.gz | Fastqsanger.gz | |||
| SRR20610761_1.fastq.gz | Fastqsanger.gz | |||
| SRR20610761_2.fastq.gz | Fastqsanger.gz | |||
| SRR20610762_1.fastq.gz | Fastqsanger.gz |
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Project description:Development of a vaccine against gonorrhoea is a global priority, driven by the rise in antibiotic resistance and the need to protect against infection and reproductive health consequences. Although Neisseria gonorrhoeae (Ng) infection does not induce substantial protective immunity, there is evidence that highly exposed individuals may develop immunity against re-infection with the same strain. In contrast, retrospective epidemiological studies have shown that immunisation with vaccines containing Neisseria meningitidis (Nm) outer membrane vesicles (OMVs) provides a degree of cross-protection against Ng infection. To examine this phenomenon, we conducted a clinical trial of 4CMenB (Bexsero®, GSK), a licensed vaccine against Nm that contains OMVs and recombinant antigens, with 50 adults in coastal Kenya who have high exposure to Ng. The study comprised a single arm open label study of two doses of Bexsero; humoral and cellular immune responses were measured at three time points over six months. Using a dedicated microarray of Ng antigens, we show that serum IgG and IgA reactivities against the gonococcal homologs of the recombinant antigens in the vaccine peaked at 10 weeks but had declined by 24 weeks. The reverse was the case for most antigens originating from the OMV component. A cohort of similar individuals with laboratory-confirmed gonococcal infection were compared before, during, and after infection: their reactivities were weaker and differed from the vaccinated cohort. We conclude that the cross-protection of the 4CMenB vaccine against gonorrhoea could be explained by cross-reaction against a diverse selection of antigens derived from the OMV component.
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Project description:The development of vaccines based on outer membrane vesicles (OMV) that naturally bud off from bacteria is an evolving field in infectious diseases. However, the inherent inflammatory nature of OMV limits their use as human vaccines. This study employed an engineered vesicle technology to develop synthetic bacterial vesicles (SyBV or aOMV) that activate the immune system without the severe immunotoxicity of OMV. SyBV were generated from bacterial membranes through treatment with detergent and ionic stress. SyBV induced less inflammatory responses in macrophages and in mice compared to natural OMV. Immunization with SyBV or OMV induced comparable antigen-specific adaptive immunity. Specifically, immunization with Pseudomonas aeruginosa-derived SyBV protected mice against bacterial challenge, and this was accompanied by significant reduction in lung cell infiltration and inflammatory cytokines. Further, immunization with Escherichia coli-derived SyBV protected mice against E. coli sepsis, comparable to OMV-immunized group. The protective activity of SyBV was driven by the stimulation of B-cell and T-cell immunity. Also, SyBV had the ability to confer cross-protection against different bacterial strain. Next, SyBV were engineered to display the SARS-CoV-2 S1 protein on their surface, and these vesicles induced specific S1 protein antibody and T-cell responses. Collectively, these results demonstrate that SyBV may be a safe and efficient vaccine platform for the prevention of bacterial and viral infections
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Project description:Sepsis causes millions of deaths per year worldwide and is a current global health priority declared by the WHO. Sepsis-related deaths are a result of dysregulated inflammatory immune responses indicating the need to develop strategies to target inflammation. An important mediator of inflammation is extracellular adenosine triphosphate (ATP) that is secreted by inflamed host cells and tissues, and also by bacteria in a strain-specific and growth phase-dependent manner. Here, we investigated the mechanisms by which bacteria release ATP. Using genetic mutant strains of Escherichia coli (E. coli), we demonstrate that ATP release is dependent on ATP synthase within the inner bacterial membrane. In addition, impaired integrity of the outer bacterial membrane and bacterial death notably contribute to ATP release. In a mouse model of abdominal sepsis, local effects of bacterial ATP were analysed using a transformed E. coli bearing an arabinose-inducible periplasmic apyrase hydrolyzing ATP to be released. Abrogating bacterial ATP release shows that bacterial ATP suppresses local immune responses, resulting in reduced neutrophil counts and impaired survival. In addition, bacterial ATP has systemic effects via its transport in outer membrane vesicles (OMV). ATP-loaded OMV are quickly distributed throughout the body and upregulated expression of genes activating degranulation in neutrophils, potentially contributing to the exacerbation of sepsis severity. This study reveals mechanisms of bacterial ATP release and its local and systemic roles in sepsis pathogenesis.
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Project description:The human gut microbe Bacteroides fragilis can alter the expression of its surface molecules such as capsular polysaccharides and SusC/SusD family outer membrane proteins through the reversible DNA inversions. We have revealed that the outer membrane vesicle (OMV) formation in B. fragilis is regulated by BF2766 (tyrosine recombinase)-mediated DNA inversions at two distantly located promoter regions previously designated as class IV regions. In this study, we aimed to identify the genetic loci associating with the OMV formation by means of transcriptome analysis on the isogenic BF2766 mutants. By comparing the transciptomes of four BF2766 deletion mutants, in which the promoter orientations in class IV-1 and IV-2 regions were locked ON/ON, OFF/ON, OFF/OFF, or ON/OFF, we found that the transcription of the genes downstream of class IV-2 markedly elevated in a hyper-vesiculating ON/ON strain.
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