Nature immunology · 2018
Inflammation induced by influenza virus impairs human innate immune control of pneumococcus.
СтатьяРандомизированное исследованиеПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Jochems Simon P, Marcon Fernando, Carniel Beatriz F, Holloway Mark, Mitsi Elena, Smith Emma, Gritzfeld Jenna F, Solórzano Carla, Reiné Jesús, Pojar Sherin, Nikolaou Elissavet, German Esther L, Hyder-Wright Angie, Hill Helen, Hales Caz, de Steenhuijsen Piters Wouter A A, Bogaert Debby, Adler Hugh, Zaidi Seher, Connor Victoria, Gordon Stephen B, Rylance Jamie, Nakaya Helder I, Ferreira Daniela M
Аннотация
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.