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

Inflammation induced by influenza virus impairs human innate immune control of pneumococcus.
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DOI:
10.1038/s41590-018-0231-y
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发表时间:
2018-12
期刊:
影响因子:
30.5
通讯作者:
Ferreira DM
Ferreira DM
中科院分区:
医学1区
文献类型:
--
作者:
Jochems SP;Marcon F;Carniel BF;Holloway M;Mitsi E;Smith E;Gritzfeld JF;Solórzano C;Reiné J;Pojar S;Nikolaou E;German EL;Hyder-Wright A;Hill H;Hales C;de Steenhuijsen Piters WAA;Bogaert D;Adler H;Zaidi S;Connor V;Gordon SB;Rylance J;Nakaya HI;Ferreira DM

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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. Pneumococcal carriage in the upper respiratory tract is an important determinant of influenza severity. Jochems et al. use human systems analysis to show that influenza-induced inflammation increases bacterial burden in the nasal cavity with implications for secondary bacterial pneumonia.
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