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

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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