Type I interferon protects against pneumococcal invasive disease by inhibiting bacterial transmigration across the lung.

Streptococcus pneumoniae infection is a leading cause of bacterial pneumonia, sepsis and meningitis and is associated with high morbidity and mortality. Type I interferon (IFN-I), whose contribution to antiviral and intracellular bacterial immunity is well established, is also elicited during pneumo...

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Autores principales:	Kim S LeMessurier, Hans Häcker, Liying Chi, Elaine Tuomanen, Vanessa Redecke
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/2fba4f496af54d92a578a2b456dc1feb
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spelling	oai:doaj.org-article:2fba4f496af54d92a578a2b456dc1feb2021-11-18T06:07:22ZType I interferon protects against pneumococcal invasive disease by inhibiting bacterial transmigration across the lung.1553-73661553-737410.1371/journal.ppat.1003727https://doaj.org/article/2fba4f496af54d92a578a2b456dc1feb2013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24244159/pdf/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Streptococcus pneumoniae infection is a leading cause of bacterial pneumonia, sepsis and meningitis and is associated with high morbidity and mortality. Type I interferon (IFN-I), whose contribution to antiviral and intracellular bacterial immunity is well established, is also elicited during pneumococcal infection, yet its functional significance is not well defined. Here, we show that IFN-I plays an important role in the host defense against pneumococci by counteracting the transmigration of bacteria from the lung to the blood. Mice that lack the type I interferon receptor (Ifnar1 (-/-)) or mice that were treated with a neutralizing antibody against the type I interferon receptor, exhibited enhanced development of bacteremia following intranasal pneumococcal infection, while maintaining comparable bacterial numbers in the lung. In turn, treatment of mice with IFNβ or IFN-I-inducing synthetic double stranded RNA (poly(I:C)), dramatically reduced the development of bacteremia following intranasal infection with S. pneumoniae. IFNβ treatment led to upregulation of tight junction proteins and downregulation of the pneumococcal uptake receptor, platelet activating factor receptor (PAF receptor). In accordance with these findings, IFN-I reduced pneumococcal cell invasion and transmigration across epithelial and endothelial layers, and Ifnar1 (-/-) mice showed overall enhanced lung permeability. As such, our data identify IFN-I as an important component of the host immune defense that regulates two possible mechanisms involved in pneumococcal invasion, i.e. PAF receptor-mediated transcytosis and tight junction-dependent pericellular migration, ultimately limiting progression from a site-restricted lung infection to invasive, lethal disease.Kim S LeMessurierHans HäckerLiying ChiElaine TuomanenVanessa RedeckePublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 9, Iss 11, p e1003727 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
spellingShingle	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 Kim S LeMessurier Hans Häcker Liying Chi Elaine Tuomanen Vanessa Redecke Type I interferon protects against pneumococcal invasive disease by inhibiting bacterial transmigration across the lung.
description	Streptococcus pneumoniae infection is a leading cause of bacterial pneumonia, sepsis and meningitis and is associated with high morbidity and mortality. Type I interferon (IFN-I), whose contribution to antiviral and intracellular bacterial immunity is well established, is also elicited during pneumococcal infection, yet its functional significance is not well defined. Here, we show that IFN-I plays an important role in the host defense against pneumococci by counteracting the transmigration of bacteria from the lung to the blood. Mice that lack the type I interferon receptor (Ifnar1 (-/-)) or mice that were treated with a neutralizing antibody against the type I interferon receptor, exhibited enhanced development of bacteremia following intranasal pneumococcal infection, while maintaining comparable bacterial numbers in the lung. In turn, treatment of mice with IFNβ or IFN-I-inducing synthetic double stranded RNA (poly(I:C)), dramatically reduced the development of bacteremia following intranasal infection with S. pneumoniae. IFNβ treatment led to upregulation of tight junction proteins and downregulation of the pneumococcal uptake receptor, platelet activating factor receptor (PAF receptor). In accordance with these findings, IFN-I reduced pneumococcal cell invasion and transmigration across epithelial and endothelial layers, and Ifnar1 (-/-) mice showed overall enhanced lung permeability. As such, our data identify IFN-I as an important component of the host immune defense that regulates two possible mechanisms involved in pneumococcal invasion, i.e. PAF receptor-mediated transcytosis and tight junction-dependent pericellular migration, ultimately limiting progression from a site-restricted lung infection to invasive, lethal disease.
format	article
author	Kim S LeMessurier Hans Häcker Liying Chi Elaine Tuomanen Vanessa Redecke
author_facet	Kim S LeMessurier Hans Häcker Liying Chi Elaine Tuomanen Vanessa Redecke
author_sort	Kim S LeMessurier
title	Type I interferon protects against pneumococcal invasive disease by inhibiting bacterial transmigration across the lung.
title_short	Type I interferon protects against pneumococcal invasive disease by inhibiting bacterial transmigration across the lung.
title_full	Type I interferon protects against pneumococcal invasive disease by inhibiting bacterial transmigration across the lung.
title_fullStr	Type I interferon protects against pneumococcal invasive disease by inhibiting bacterial transmigration across the lung.
title_full_unstemmed	Type I interferon protects against pneumococcal invasive disease by inhibiting bacterial transmigration across the lung.
title_sort	type i interferon protects against pneumococcal invasive disease by inhibiting bacterial transmigration across the lung.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/2fba4f496af54d92a578a2b456dc1feb
work_keys_str_mv	AT kimslemessurier typeiinterferonprotectsagainstpneumococcalinvasivediseasebyinhibitingbacterialtransmigrationacrossthelung AT hanshacker typeiinterferonprotectsagainstpneumococcalinvasivediseasebyinhibitingbacterialtransmigrationacrossthelung AT liyingchi typeiinterferonprotectsagainstpneumococcalinvasivediseasebyinhibitingbacterialtransmigrationacrossthelung AT elainetuomanen typeiinterferonprotectsagainstpneumococcalinvasivediseasebyinhibitingbacterialtransmigrationacrossthelung AT vanessaredecke typeiinterferonprotectsagainstpneumococcalinvasivediseasebyinhibitingbacterialtransmigrationacrossthelung
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Type I interferon protects against pneumococcal invasive disease by inhibiting bacterial transmigration across the lung.

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