Increased pathogenicity of pneumococcal serotype 1 is driven by rapid autolysis and release of pneumolysin
Laura C. Jacques,
Stavros Panagiotou,
Murielle Baltazar,
Madikay Senghore,
Shadia Khandaker,
Rong Xu,
Laura Bricio-Moreno,
Marie Yang,
Christopher G. Dowson,
Dean B. Everett,
Daniel R. Neill and
Aras Kadioglu ()
Additional contact information
Laura C. Jacques: Department of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool
Stavros Panagiotou: Department of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool
Murielle Baltazar: Department of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool
Madikay Senghore: Medical Research Council Unit, The Gambia
Shadia Khandaker: Department of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool
Rong Xu: Department of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool
Laura Bricio-Moreno: Department of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool
Marie Yang: Department of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool
Christopher G. Dowson: School of Life Sciences, University of Warwick
Dean B. Everett: Malawi-Liverpool-Wellcome Trust Clinical Research Programme, University of Malawi, College of Medicine
Daniel R. Neill: Department of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool
Aras Kadioglu: Department of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool
Nature Communications, 2020, vol. 11, issue 1, 1-13
Abstract:
Abstract Streptococcus pneumoniae serotype 1 is the predominant cause of invasive pneumococcal disease in sub-Saharan Africa, but the mechanism behind its increased invasiveness is not well understood. Here, we use mouse models of lung infection to identify virulence factors associated with severe bacteraemic pneumonia during serotype-1 (ST217) infection. We use BALB/c mice, which are highly resistant to pneumococcal pneumonia when infected with other serotypes. However, we observe 100% mortality and high levels of bacteraemia within 24 hours when BALB/c mice are intranasally infected with ST217. Serotype 1 produces large quantities of pneumolysin, which is rapidly released due to high levels of bacterial autolysis. This leads to substantial levels of cellular cytotoxicity and breakdown of tight junctions between cells, allowing a route for rapid bacterial dissemination from the respiratory tract into the blood. Thus, our results offer an explanation for the increased invasiveness of serotype 1.
Date: 2020
References: Add references at CitEc
Citations:
Downloads: (external link)
https://www.nature.com/articles/s41467-020-15751-6 Abstract (text/html)
Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.
Export reference: BibTeX
RIS (EndNote, ProCite, RefMan)
HTML/Text
Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-15751-6
Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/
DOI: 10.1038/s41467-020-15751-6
Access Statistics for this article
Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie
More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().