期刊
NATURE COMMUNICATIONS
卷 10, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-019-11005-2
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资金
- Wellcome Trust [106846/Z/15/Z]
- NIHR Global Health Research Unit on Mucosal Pathogens [16/136/46]
- Medical Research Council [MR/M011569/1]
- Bill and Melinda Gates Foundation [OPP1117728]
- National Institute for Health Research (NIHR) Local Comprehensive Research Network
- Wellcome Trust Multi-User Equipment Grant [104936/Z/14/Z]
- MRC [G0900950]
- NIHR Biomedical Research Centre
- Wellcome Trust
- UCL/UCLH Biomedical Research Centre
- MRC [MR/N02687X/1, G0900950, MR/M011569/1] Funding Source: UKRI
Control of Streptococcus pneumoniae colonisation at human mucosal surfaces is critical to reducing the burden of pneumonia and invasive pneumococcal disease, interrupting transmission, and achieving herd protection. Here, we use an experimental human pneumococcal carriage model (EHPC) to show that S. pneumoniae colonisation is associated with epithelial surface adherence, micro-colony formation and invasion, without overt disease. Interactions between different strains and the epithelium shaped the host transcriptomic response in vitro. Using epithelial modules from a human epithelial cell model that recapitulates our in vivo findings, comprising of innate signalling and regulatory pathways, inflammatory mediators, cellular metabolism and stress response genes, we find that inflammation in the EHPC model is most prominent around the time of bacterial clearance. Our results indicate that, rather than being confined to the epithelial surface and the overlying mucus layer, the pneumococcus undergoes micro-invasion of the epithelium that enhances inflammatory and innate immune responses associated with clearance.
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