Studies have demonstrated that the development of ALI/ARDS leads to excessive production of proinflammatory cytokines, such as tumour necrosis factor (TNF)-n, interleukin (IL)-1rl IL-6, and IL-8, by immune cells [8], and chemotactic inflammatory cells excessively infiltrate lung tissue, resulting in oedema and gas exchange deterioration [9]. Here, IL6 is linked to acute respiratory distress syndrome.