Cigarette smoke exposure redirects Staphylococcus aureus to a virulence profile associated with persistent infection
Lacoma, Alicia (Institut Germans Trias i Pujol. Hospital Universitari Germans Trias i Pujol)
Edwards, A. M. (MRC Centre for Molecular Bacteriology and Infection. Imperial College London)
Young, Bernadette (Nuffield Department of Medicine. Experimental Medicine Division. University of Oxford)
Domínguez, José (Institut Germans Trias i Pujol. Hospital Universitari Germans Trias i Pujol)
Prat i Aymerich, Cristina (Institut Germans Trias i Pujol. Hospital Universitari Germans Trias i Pujol)
Laabei, Maisem (Institut Germans Trias i Pujol. Hospital Universitari Germans Trias i Pujol)
Universitat Autònoma de Barcelona

Data:	2019
Resum:	Tobacco smoking represents the leading preventable cause of death worldwide. Smoking is a recognised risk factor for several pathologies and is detrimental to host immune surveillance and defence. However, the impact of smoking on microbial residents of the nasopharyngeal cavity, in contact with cigarette smoke (CS), is lacking. Staphylococcus aureus is a major human pathogen that colonises the human nasopharynx and causes a wide range of infections. We investigated the impact of CS on specific virulence phenotypes important in S aureus pathogenesis. We observed strain-dependent differences following exposure to CS, namely growth inhibition, augmented biofilm formation, increased invasion of, and persistence within, bronchial alveolar epithelial cells. Additionally, we confirm the critical role of a functional accessory gene regulator (Agr) system in mediating increased biofilm development and host cell invasion and persistence following CS exposure. Furthermore, CS exposure resulted in reduced toxin production. Importantly, exposure of S aureus to CS accelerated the frequency of mutations and resulted in a significant increase in gentamicin-resistant small colony variant (SCV) formation. Mutational analysis revealed that CS induced SCVs emerge via the SOS response DNA mutagenic repair system. Taken together, our results suggest that CS redirects certain S aureus strains to a virulence profile associated with persistence.
Ajuts:	Instituto de Salud Carlos III PI13-01418 Instituto de Salud Carlos III PI17-01139
Nota:	Altres ajuts: This work also received a grant from the Spanish Society of Pneumology and Thoracic Surgery (SEPAR 024/2016). M.L. gratefully acknowledges funding from the European Respiratory Society Long-term Fellowship grant (LTRF-5934). A.M.E. acknowledges funding from the Royal Society, Department of Medicine (Imperial College), and from the Imperial NIHR Biomedical Research Centre, Imperial College London. B.C.Y is funded by an NIHR Clinical Lectureship. CP acknowledges Programa Germans Trias Sapiens Fundació Catalunya la Pedrera and European Respiratory Society short term research fellowship October 2018 (STRTF201810-00467).
Drets:	Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.
Llengua:	Anglès
Document:	Article ; recerca ; Versió publicada
Matèria:	Applied microbiology ; Pathogens
Publicat a:	Scientific reports, Vol. 9 Núm. 1 (january 2019) , p. 10798, ISSN 2045-2322

DOI: 10.1038/s41598-019-47258-6
PMID: 31346202

15 p, 1.9 MB

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Documents de recerca > Documents dels grups de recerca de la UAB > Centres i grups de recerca (producció científica) > Ciències de la salut i biociències > Institut d'Investigació en Ciencies de la Salut Germans Trias i Pujol (IGTP)
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