We and others have shown that Toll-like receptor 2 (TLR2), a membrane surface receptor that recognizes bacterial lipopeptides and lipoteichoic acid, is required and sufficient for RV-induced proinflammatory responses in vitro and in vivo.
TLR2 is required for early inflammatory responses induced by rhinovirus, and TLR2<sup>+</sup> macrophages are sufficient to confer airway inflammation to TLR2<sup>-/-</sup> mice, with the pattern of inflammation depending on the macrophage activation state.
Knockdown of TLR2, but not other MyD88-dependent TLRs, also restored IRAK-1, suggesting that TLR2 is required for RV-induced IRAK-1 degradation.In conclusion, we demonstrate for the first time that RV infection delays bacterial clearance in vivo and suppresses NTHi-stimulated chemokine responses via degradation of IRAK-1.