In conclusion, our results show that (a) enhancing the levels of TTP is protective against endotoxin-induced ALI; (b) the protective effect seen in TTPΔARE mice is attributable to reduced neutrophilic recruitment and, in turn, reduced lung damage; (c) reduced neutrophilic recruitment is attributed to reduced secretion of chemoattractants, particularly KC and G-CSF; and that, (d) TTP in non-HPCs plays an essential role in protection against endotoxin-induced ALI. The gene discussed is ZFP36; the disease is acute respiratory distress syndrome.