Holding the Inflammatory System in Check: TLRs and Their Targeted Therapy in Asthma

Figure 1

Schematic overview of TLR signaling pathway in neutrophilic and eosinophilic asthma. Gram-negative and Gram-positive bacteria as well as respiratory viruses (e.g., rhinovirus) are detected by TLRs. Subsequently, TLR3 and TLR7/8 trigger TRIF and MyD88 pathways, respectively, followed by the transcription of NF-κB in nucleus and the production of IL-4, IL-5, and IL-13, inducing eosinophilic asthma. TLR2 and TLR4 induce MyD88 and MyD88 as well as TRIF cascades, respectively, followed by the transcriptions of MAPK and NF-κB into nucleus, triggering the release of IL-1β and IL-8 and the onset of neutrophilic asthma. MAPK: mitogen-activated protein kinase; MyD88: myeloid differentiation primary-response gene 88; NF-κB: nuclear factor-κB; TLR: Toll-like receptor; TRIF: Toll/IL-1R (TIR) domain containing adaptor protein inducing IFN-β.