IL10 and acute respiratory distress syndrome: Clinical features of the disease thus far have shown to be an initial increase in the secretion of interleukin (IL)–4 and IL-10, which are T helper (Th)–2 cytokines and suppress inflammation ([37] as cited in [38]), and a Th-1 cell hyper-response that is thought to lead to the ARDS associated with severe acute respiratory syndrome (SARS; [39] as cited in [38]).