TLR4 and Sepsis: TLR4 responds stronglyto the presence of lipid A, the most conserved part of LPS, leadingto the activation of transcription factors NF-κB and IRF-3,and triggers the biosynthesis of various inflammation mediators suchas IL-1β, TNF, IFNs, and IL-6. Additionally,LPS is an essential factor in the induction of ROS synthesis and NETs formation in neutrophils. Moreover, excessive systemic exposure to LPScan lead to severe sepsis, potentially resulting in the host’sdeath.