TLR4, once bound to its ligand LPS, activates nuclear factor-κB (NF-κB), which subsequently causes the secretion of pro-inflammatory cytokines such as interleukin-1β (IL-1β), IL-6 and tumor necrosis factor-alpha (TNF-α) (10–13), leading to a series of inflammatory reactions to resist LPS infection (14–16). Here, TNF is linked to infection.