In support of this hypothesis, it has been shown that infection of airway epithelial cells with Hemophilus influenza induced the secretion of CXCL-8, up regulated TLR3 expression and increased the responsiveness to a secondary challenge of Rhinovirus. Interestingly, inhibition of TLR3 with small interfering RNA, inhibited the Rhinovirus-induced CXCL-8 production [17]. Here, TLR3 is linked to infection.