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Blood. 2011 Nov 3;118(18):5050-9. doi: 10.1182/blood-2011-03-343293. Epub 2011 Aug 25.

Angiopoietin-2 promotes myeloid cell infiltration in a β₂-integrin-dependent manner.

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Edinger Institute/Institute of Neurology, Frankfurt University Medical School, Frankfurt, Germany.


In human inflammatory diseases, we identified endothelial angiopoietin-2 (Ang-2) expression to be strongly associated with inflammations mediated by myeloid cells but not lymphocytes. To identify the underlying mechanism, we made use of a transgenic mouse model with inducible endothelial cell-specific expression of Ang-2. In this model, in the absence of inflammatory stimuli, long-term expression of Ang-2 led to a time-dependent accumulation of myeloid cells in numerous organs, suggesting that Ang-2 is sufficient to recruit myeloid cells. In models of acute inflammation, such as delayed-type hypersensitivity and peritonitis, Ang-2 transgenic animals showed an increased responsiveness. Intravital fluorescence video microscopy revealed augmented cell adhesion as an underlying event. Consequently, we demonstrated that Ang-2 is able to induce strong monocyte adhesion under shear in vitro, which could be blocked by antibodies to β₂-integrin. Taken together, our results describe Ang-2 as a novel, endothelial-derived regulator of myeloid cell infiltration that modulates β₂-integrin-mediated adhesion in a paracrine manner.

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