Physiological lung dysfunction was accompanied by alteration in alveolar-capillary barrier permeability on 8 and 9 dpi and confirmed by the increase of protein concentration in BALF, due to extravasation of plasma protein to the lungs observed on day 9 post-infection, as previously observed on PbANKA [43] and PbNK65 experimental models [23], as well as influx of mononuclear cells and increased levels of MCP-1 on BALF. The gene discussed is CCL2; the disease is infection.