Therefore, in the present study, either Leptin in BAL acted anti-inflammatory and prevented an increased particle related neutrophil influx in CA and HF mice, or, if BAL Leptin action was pro-inflamamtory, then other molecular factors may have counterbalanced, like the reduced MIP2 and IFNγ concentrations in BAL, which predominantly can be dedicated to be of alveolar macrophage origin. The gene discussed is IFNG; the disease is hydrops fetalis.