<named-content content-type="genus-species">Staphylococcus aureus</named-content> and Influenza A Virus: Partners in Coinfection

ABSTRACT Nasal carriage of Staphylococcus aureus is a significant risk factor for secondary staphylococcal pneumonia in influenza A virus (IAV)-infected hosts. However, little research has been undertaken to define the environmental and physiological changes that cause S. aureus to shift from commen...

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Autores principales:	Michelle E. Mulcahy, Rachel M. McLoughlin
Formato:	article
Lenguaje:	EN
Publicado:	American Society for Microbiology 2016
Materias:	Microbiology QR1-502
Acceso en línea:	https://doaj.org/article/2d6afc31c2e34a45adffba38d2cdb363
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spelling	oai:doaj.org-article:2d6afc31c2e34a45adffba38d2cdb3632021-11-15T15:50:16Z<named-content content-type="genus-species">Staphylococcus aureus</named-content> and Influenza A Virus: Partners in Coinfection10.1128/mBio.02068-162150-7511https://doaj.org/article/2d6afc31c2e34a45adffba38d2cdb3632016-12-01T00:00:00Zhttps://journals.asm.org/doi/10.1128/mBio.02068-16https://doaj.org/toc/2150-7511ABSTRACT Nasal carriage of Staphylococcus aureus is a significant risk factor for secondary staphylococcal pneumonia in influenza A virus (IAV)-infected hosts. However, little research has been undertaken to define the environmental and physiological changes that cause S. aureus to shift from commensal to pathogenic organism in this setting. The ability of virus-driven danger signals to cause S. aureus to transition from commensalism to pulmonary infection was explored in a recent study by Reddinger et al. R. M. Reddinger, N. R. Luke-Marshall, A. P. Hakansson, and A. A. Campagnari, mBio 7(6):e01235-16, 2016, http://dx.doi.org/10.1128/mBio.01235-16. The authors report that physiological host changes, including febrile temperature and a combination of host stress response signals, caused S. aureus biofilms to disperse from the nasal environment and cause active pulmonary infection. This commentary discusses the new finding in light of the current understanding of the mechanisms behind staphylococcal coinfection with IAV. In addition, it considers the mechanisms behind staphylococcal dispersal in this model. Overall, the study indicates that interkingdom signaling may occur following IAV infection and this likely contributes to sensitizing the IAV-infected host to secondary staphylococcal pneumonia.Michelle E. MulcahyRachel M. McLoughlinAmerican Society for MicrobiologyarticleMicrobiologyQR1-502ENmBio, Vol 7, Iss 6 (2016)
institution	DOAJ
collection	DOAJ
language	EN
topic	Microbiology QR1-502
spellingShingle	Microbiology QR1-502 Michelle E. Mulcahy Rachel M. McLoughlin <named-content content-type="genus-species">Staphylococcus aureus</named-content> and Influenza A Virus: Partners in Coinfection
description	ABSTRACT Nasal carriage of Staphylococcus aureus is a significant risk factor for secondary staphylococcal pneumonia in influenza A virus (IAV)-infected hosts. However, little research has been undertaken to define the environmental and physiological changes that cause S. aureus to shift from commensal to pathogenic organism in this setting. The ability of virus-driven danger signals to cause S. aureus to transition from commensalism to pulmonary infection was explored in a recent study by Reddinger et al. R. M. Reddinger, N. R. Luke-Marshall, A. P. Hakansson, and A. A. Campagnari, mBio 7(6):e01235-16, 2016, http://dx.doi.org/10.1128/mBio.01235-16. The authors report that physiological host changes, including febrile temperature and a combination of host stress response signals, caused S. aureus biofilms to disperse from the nasal environment and cause active pulmonary infection. This commentary discusses the new finding in light of the current understanding of the mechanisms behind staphylococcal coinfection with IAV. In addition, it considers the mechanisms behind staphylococcal dispersal in this model. Overall, the study indicates that interkingdom signaling may occur following IAV infection and this likely contributes to sensitizing the IAV-infected host to secondary staphylococcal pneumonia.
format	article
author	Michelle E. Mulcahy Rachel M. McLoughlin
author_facet	Michelle E. Mulcahy Rachel M. McLoughlin
author_sort	Michelle E. Mulcahy
title	<named-content content-type="genus-species">Staphylococcus aureus</named-content> and Influenza A Virus: Partners in Coinfection
title_short	<named-content content-type="genus-species">Staphylococcus aureus</named-content> and Influenza A Virus: Partners in Coinfection
title_full	<named-content content-type="genus-species">Staphylococcus aureus</named-content> and Influenza A Virus: Partners in Coinfection
title_fullStr	<named-content content-type="genus-species">Staphylococcus aureus</named-content> and Influenza A Virus: Partners in Coinfection
title_full_unstemmed	<named-content content-type="genus-species">Staphylococcus aureus</named-content> and Influenza A Virus: Partners in Coinfection
title_sort	<named-content content-type="genus-species">staphylococcus aureus</named-content> and influenza a virus: partners in coinfection
publisher	American Society for Microbiology
publishDate	2016
url	https://doaj.org/article/2d6afc31c2e34a45adffba38d2cdb363
work_keys_str_mv	AT michelleemulcahy namedcontentcontenttypegenusspeciesstaphylococcusaureusnamedcontentandinfluenzaaviruspartnersincoinfection AT rachelmmcloughlin namedcontentcontenttypegenusspeciesstaphylococcusaureusnamedcontentandinfluenzaaviruspartnersincoinfection
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<named-content content-type="genus-species">Staphylococcus aureus</named-content> and Influenza A Virus: Partners in Coinfection

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