Pretreatment with 1,7-dimethylxanthine (or paraxanthine) inhibited a PARP-1 activity that plays an important role in LPS-induced lung inflammation, lowered lung MPO levels, transcription of IL-6, TNFα, macrophage inflammatory protein (MIP)1α and MIP2 genes and PAR-polymer formation, and reduced markers of systemic inflammation (serum amyloid P component and IL-6) in LPS-induced ALI [48]. Here, CXCL2 is linked to acute respiratory distress syndrome.