Genomic features of predominant non-PCV13 serotypes responsible for adult invasive pneumococcal disease in Spain
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ABSTRACT:
PROVIDER: PRJEB50014 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| ERR7977540_1.fastq.gz | Fastqsanger.gz | |||
| ERR7977540_2.fastq.gz | Fastqsanger.gz | |||
| ERR7977550_1.fastq.gz | Fastqsanger.gz | |||
| ERR7977550_2.fastq.gz | Fastqsanger.gz |
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Project description:Pneumococcal infections cause serious illness and death among older adults. A capsular polysaccharide vaccine PPSV23 (Pneumovax®) and a conjugated polysaccharide vaccine PCV13 (Prevnar®) are used to prevent these infections, yet underlying immunological responses, and baseline predictors remain unknown. We recruited and vaccinated 39 older adults (>60 years) with PPSV23 or PCV13. Both vaccines induced strong antibody responses at day 28 and similar plasmablast transcriptional signatures at day 10, however, their baseline predictors were distinct. Analyses of baseline flow cytometry and RNA-seq data (bulk and single cell) revealed a novel baseline phenotype that is specifically associated with weaker PCV13 responses, characterized by i) increased expression of cytotoxicity-associated genes and increased CD16+ NK frequency; ii) increased Th17 and decreased Th1 cell frequency. Men were more likely to display this cytotoxic phenotype and mounted weaker responses to PCV13 than women. Baseline expression levels of a distinct gene set was predictive of PPSV23 responses. This first precision vaccinology study for pneumococcal vaccine responses of older adults uncovered novel and distinct baseline predictors that might transform vaccination strategies and initiate novel interventions.
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Project description:Background: Pneumococcal secondary infection following influenza A virus (IAV) pneumonia is a synergistic complication with high mortality. While varying invasiveness of pneumococcal serotypes is an important pathogenic factor, serotype-specifc immediate-early transcriptional responses of the IAV-perturbed alveolar epithelium have not been adressed. We comprehensively analyzed gene transcription in alveolar type II epithelial cells (AECII) isolated from mice infected with IAV and/or S. pneumoniae (S.pn.) serotypes 4, 7F and 19F. Results: IAV, 14 days post infection, rendered the lung susceptible to invasive secondary S.pn. infection with serotypes 4 and 7F but not 19F. Only secondary 7F infection induced exacerbated cytokine/chemokine responses. IAV/7F infection induced superior protein expression of type I and II interferons, acesserbated expression in IAV/serotype 4 infection. Inference of a scale-free-like ARACNE gene co-expression network revealed interferon-response network modules in AECII and network-mapping unfolded S.pn. serotype-specific transcriptional network responses/usage. Secondary S.pn. infection abrogated the IAV-induced pneumocyte proliferative configuration and preceeding IAV infection rendered the transcriptional response to 7F infection comparable to that towards serotype 4. This related especially to network genes correlating with the expression of two master regulators of interferon responses: Irf7 and Stat1. Epigenetic ATAC-seq analysis of AECII in resolved IAV infection identified enhanced expression of ARACNE network genes Hist1h2bf, Igtp, Mki67, Rasl10b, H2-Q6 and H2-Q7 to be associated with increased chromatin accessability at promoter regions. Conclusions: We show that AECII sustainably retain an IAV-associated transcriptional configuration with epigenetic involvement, that serotype-specifically affects proliferation and accelerates and enhances the AECII transcriptional response, mainly to interferons, in secondary S.pn. infection.
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