In ALI, in vivo experiments demonstrated that TLR9 contributes to the development of ALI and systemic inflammation, and inhibition of TLR9 prominently attenuated histopathological changes and pro-inflammatory mediators, including interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor–α (TNF-α) (50, 109–114). Here, IL1B is linked to acute respiratory distress syndrome.