These data suggest that gpx-1 primes pro-inflammatory cytokine production after LPS challenge in vivo and suggest the possible therapeutic utility of blocking gpx-1 in human lung diseases where high neutrophil and macrophage numbers, protease induction, and TNF-α, MIP-2 and GM-CSF overproduction are believed to be central agents in disease pathogenesis. Here, CSF2 is linked to lung disorder.