Increased pathogenicity of pneumococcal serotype 1 is driven by rapid autolysis and release of pneumolysin



Jacques, Laura C, Panagiotou, Stavros ORCID: 0000-0001-9972-5068, Baltazar, Murielle ORCID: 0000-0002-1972-2308, Senghore, Madikay, Khandaker, Shadia, Xu, Rong, Bricio-Moreno, Laura, Yang, Marie, Dowson, Christopher G, Everett, Dean B
et al (show 2 more authors) (2020) Increased pathogenicity of pneumococcal serotype 1 is driven by rapid autolysis and release of pneumolysin. NATURE COMMUNICATIONS, 11 (1). 1892-.

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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.

Item Type: Article
Uncontrolled Keywords: Lung, Nasopharynx, Epithelial Cells, Animals, Mice, Inbred BALB C, Humans, Mice, Streptococcus pneumoniae, Bacteremia, Pneumococcal Infections, Disease Models, Animal, Autolysis, Bacterial Proteins, Bacterial Toxins, Streptolysins, Virulence Factors, Virulence, Cell Survival, Female, Serogroup, A549 Cells
Depositing User: Symplectic Admin
Date Deposited: 24 Apr 2020 11:22
Last Modified: 18 Jan 2023 23:53
DOI: 10.1038/s41467-020-15751-6
Related URLs:
URI: https://livrepository.liverpool.ac.uk/id/eprint/3084576