Lipopolysaccharide (LPS) and pro-inflammatory cytokines can shift the Ang/Tie balance, rouse ECs from quiescence and provoke an inflammatory response. In rodents LPS injection induces expression of Ang-2 mRNA and protein and reduces the levels of Ang-1, Tie2 and Tie2 phosphorylation in lung, liver and diaphragm within 24 hours, which may promote or maintain vascular leakage. The initial increase in permeability is probably due to release of Ang-2 stored in WPBs [39, 128] . In a mouse model of LPS-induced lung injury, pulmonary oedema was found to be related to the balance between VEGF, Ang-1 and Ang-4 [129] . In a comparable model, Ang-1-producing transfected cells reduced alveolar inflammation and leakage [130] .