Local IL-17A potentiates early neutrophil recruitment to the respiratory tract during severe RSV infection.

Respiratory syncytial virus (RSV) bronchiolitis triggers a strong innate immune response characterized by excessive neutrophil infiltration which contributes to RSV induced pathology. The cytokine IL-17A enhances neutrophil infiltration into virus infected lungs. IL-17A is however best known as an effector of adaptive immune responses.

Defective control of vitamin D receptor-mediated epithelial STAT1 signalling predisposes to severe respiratory syncytial virus bronchiolitis.

Respiratory syncytial virus (RSV) infection causes bronchiolitis in infants with seasonal frequency, for which vitamin D deficiency and a well-described polymorphism in the vitamin D receptor (VDR) FokI are important risk factors. Recent studies suggest that vitamin D regulates immune pathways in airway epithelial cells during RSV infection. It is not understood why the VDR FokI polymorphism predisposes to severe RSV bronchiolitis.