IL1B and acute respiratory distress syndrome: LPS specifically activates TLRs, leading to activation of the nuclear factor-kappa B (NF-κB) signaling pathway, and secretion of pro-inflammatory cytokines and chemokines, such as interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor α (TNF-α) and type 1 interferons [7,8], whose overproduction is associated with a development of acute respiratory distress syndrome (ARDS) [9,10].