TLR4 and fungal infectious disease: Furthermore, they promote the production of reactive oxygen species, which then activate the TLR4/NF-κB pathway, boost the production of inflammatory substances (TNF-α, IL-1β and IL-6), accelerate apoptosis (Bax/Bcl-2) and ultimately result in heightened tissue harm and susceptibility to bacterial, viral and fungal infections 46,47.