FIG. 3.

Schematic overview. We previously demonstrated that recognition of NTHi is mediated by CD14 and TLR4 (17). Subsequently, it was reported that the MyD88-dependent route of TLR4 signaling enhances the inflammatory response and bacterial clearance (17). Moreover, we demonstrated that host defense against NTHi was not dependent on TNF or the platelet-activating factor (3, 9). Here, we found that the MyD88-dependent IL-18 is important for the inflammatory response and antibacterial host defense. It will be of interest to determine the role of IL-1, whose signaling is also dependent on MyD88, in this experimental model.