Once engaged, PRRs fuel the expression of NF-κB driven cytokine and chemokine expression (e.g., tumor necrosis factor-α (TNFα), interleukin-1β (IL-1β), IL-8, IL-6) [63], which promotes autophagy and apoptosis and induces the expression of TLRs, which are intimately involved with development of ARDS. This evidence concerns the gene CXCL8 and acute respiratory distress syndrome.