Desialylation of airway epithelial cells during influenza virus infection enhances pneumococcal adhesion via galectin binding
Review articleOpen access

Highlights•We studied the role of galectins in pneumococcal adhesion in the lung upon influenza.•After influenza, galectin-1 and -3 levels are increased in the bronchoalveolar space.•Viral and bacterial neuraminidases increase galectin binding to epithelial cells.•Galectin-1 and -3 bind to glycans from the influenza virus and pneumococcus.•Galectin-3 enhances pneumococcal adhesion to influenza-infected airway epithelium.

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