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Sci Rep. 2018 Oct 24;8(1):15716. doi: 10.1038/s41598-018-34103-5.

The transcriptomic response of Streptococcus pneumoniae following exposure to cigarette smoke extract.

Author information

1
Pneumococcal Research, Murdoch Children's Research Institute, Infection and Immunity, Parkville, 3052, Australia. sam.manna@mcri.edu.au.
2
Pneumococcal Research, Murdoch Children's Research Institute, Infection and Immunity, Parkville, 3052, Australia.
3
Chronic Infectious and Inflammatory Disease Programme, School of Health & Biomedical Sciences, RMIT University, Bundoora, 3083, Australia.
4
Department of Animal, Plant and Soil Sciences, La Trobe University, Melbourne, Victoria, 3086, Australia.
5
Department of Paediatrics, The University of Melbourne, Parkville, 3052, Australia.
6
Department of Microbiology and Immunology, The University of Melbourne at the Peter Doherty Institute for Infection and Immunity, Parkville, 3010, Australia.

Abstract

Exposure to cigarette smoke is a risk factor for respiratory diseases. Although most research has focused on its effects on the host, cigarette smoke can also directly affect respiratory pathogens, in some cases enhancing virulence. Streptococcus pneumoniae (the pneumococcus) is a leading cause of community-acquired pneumonia worldwide, however data on the effects of cigarette smoke on the pneumococcus are sparse. Using RNA-seq, we show that pneumococci exposed to cigarette smoke extract in a concentrated acute exposure in vitro model initiate a 'survival' transcriptional response including the upregulation of detoxification enzymes, efflux pumps and osmoregulator transporters, as well as the downregulation of fatty acid and D-alanyl lipoteichoic acid biosynthesis genes. Except for the downregulation of the pneumolysin gene, there were no changes in the expression of major virulence factors following exposure to cigarette smoke. Compared to unexposed pneumococci, smoke-exposed pneumococci did not exhibit any changes in viability, adherence, hydrophobicity or cell lysis susceptibility. In this study, we demonstrate that pneumococci adapt to acute noxious cigarette smoke exposure by inducing a gene expression signature that allows the bacteria to resist its harmful effects.

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