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Nat Immunol. 2018 Dec;19(12):1299-1308. doi: 10.1038/s41590-018-0231-y. Epub 2018 Oct 29.

Inflammation induced by influenza virus impairs human innate immune control of pneumococcus.

Author information

1
Department of Clinical Sciences, Liverpool School of Tropical Medicine, Liverpool, UK. simon.jochems@lstmed.ac.uk.
2
Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of São Paulo, São Paolo, Brazil.
3
Department of Clinical Sciences, Liverpool School of Tropical Medicine, Liverpool, UK.
4
Royal Liverpool and Broadgreen University Hospital, Liverpool, UK.
5
Centre for Inflammation Research, University of Edinburgh, Edinburgh, UK.
6
Department of Paediatric Immunology and Infectious Diseases, University Medical Center Utrecht, Utrecht, The Netherlands.
7
Department of Medical Microbiology, University Medical Center Utrecht, Utrecht, The Netherlands.
8
Malawi-Liverpool-Wellcome Trust Clinical Research Programme, Blantyre, Malawi.
9
Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of São Paulo, São Paolo, Brazil. hnakaya@usp.br.
10
Department of Clinical Sciences, Liverpool School of Tropical Medicine, Liverpool, UK. daniela.ferreira@lstmed.ac.uk.

Abstract

Colonization of the upper respiratory tract by pneumococcus is important both as a determinant of disease and for transmission into the population. The immunological mechanisms that contain pneumococcus during colonization are well studied in mice but remain unclear in humans. Loss of this control of pneumococcus following infection with influenza virus is associated with secondary bacterial pneumonia. We used a human challenge model with type 6B pneumococcus to show that acquisition of pneumococcus induced early degranulation of resident neutrophils and recruitment of monocytes to the nose. Monocyte function was associated with the clearance of pneumococcus. Prior nasal infection with live attenuated influenza virus induced inflammation, impaired innate immune function and altered genome-wide nasal gene responses to the carriage of pneumococcus. Levels of the cytokine CXCL10, promoted by viral infection, at the time pneumococcus was encountered were positively associated with bacterial load.

PMID:
30374129
PMCID:
PMC6241853
DOI:
10.1038/s41590-018-0231-y
[Indexed for MEDLINE]
Free PMC Article

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