About: Inflammation induced by influenza virus impairs innate control of human pneumococcal carriage

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About: Inflammation induced by influenza virus impairs innate control of human pneumococcal carriage Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Inflammation induced by influenza virus impairs innate control of human pneumococcal carriage
Creator	Bogaert, Debby Holloway, Mark Mitsi, Elena Pojar, Sherin Adler, Hugh Connor, Victoria Hales, Caz Hill, Helen Hyder-Wright, Angie Marcon, Fernando Reiné, Jesús Smith, Emma Solórzano, Carla Zaidi, Seher Carniel, Beatriz Ferreira, Daniela German, Esther Jochems, Simon Nakaya, Helder Daniela, Dr De, Wouter Ferreira, M Gritzfeld, Jenna Piters, Steenhuijsen
Source	BioRxiv; MedRxiv
abstract	Secondary bacterial pneumonia following influenza infection is a significant cause of mortality worldwide. Upper respiratory tract pneumococcal carriage is important as both determinants of disease and population transmission. The immunological mechanisms that contain pneumococcal carriage are well-studied in mice but remain unclear in humans. Loss of this control of carriage following influenza infection is associated with secondary bacterial pneumonia during seasonal and pandemic outbreaks. We used a human type 6B pneumococcal challenge model to show that carriage acquisition induces early degranulation of resident neutrophils and recruitment of monocytes to the nose. Monocyte function associated with clearance of pneumococcal carriage. Prior nasal infection with live attenuated influenza virus induced inflammation, impaired innate function and altered genome-wide nasal gene responses to pneumococcal carriage. Levels of the cytokine IP-10 promoted by viral infection at the time of pneumococcal encounter was positively associated with bacterial density. These findings provide novel insights in nasal immunity to pneumococcus and viral-bacterial interactions during co-infection.
has issue date	2018-06-20(xsd:dateTime)
bibo:doi	10.1101/347161
has license	biorxiv
sha1sum (hex)	dc3d8b94ae9acb1ec585507d0d77164a7f688d10
schema:url	https://doi.org/10.1101/347161
resource representing a document's title	Inflammation induced by influenza virus impairs innate control of human pneumococcal carriage
schema:publication	bioRxiv
resource representing a document's body	covid:dc3d8b94ae9acb1ec585507d0d77164a7f688d10#body_text
is schema:about of	named entity 'humans' named entity 'carriage' named entity 'carriage' named entity 'Inflammation' covid:arg/dc3d8b94ae9acb1ec585507d0d77164a7f688d10 named entity 'transmission' named entity 'pneumococcal' named entity 'degranulation' named entity 'nose' named entity 'infection' named entity 'secondary' named entity 'determinants' named entity 'influenza' named entity 'influenza infection' named entity 'pandemic outbreaks' named entity 'Monocyte' named entity 'pneumococcal' named entity 'pneumococcal' named entity 'carriage' named entity 'monocytes' named entity 'Treg' named entity 'IP-10' named entity 'MCP-1' named entity 'neutrophil' named entity 'monocyte' named entity 'randomised controlled trial' named entity 'peer-reviewed' named entity 'cytokines' named entity 'cell function' named entity 'MCP-1' named entity 'peer-reviewed' named entity 'TNF-α' named entity 'interferon' named entity 'macrophages' named entity 'pneumococcal' named entity 'monocytes' named entity 'co-expression' named entity 'differentially expressed genes' named entity 'Quality control' named entity 'S4c' named entity 'LAIV' named entity 'neutrophils' named entity 'murine models' named entity 'pneumococcal' named entity 'microbiology' named entity 'MCP-1' named entity 'bioRxiv' named entity 'neutrophil' named entity 'O-glycosylation' named entity 'murine models' named entity 'monocyte' named entity 'inoculation' named entity 'LAIV' named entity 'LAIV' named entity 'cytokines' named entity 'monocyte' named entity 'inoculation' named entity 'LAIV' named entity 'cytokine' named entity 'environmental factors' named entity 'pneumococcal'

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