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Expression of vascular adhesion protein-1 in normal and inflamed mice lungs and normal human lungs

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Abstract

Recently, vascular adhesion protein-1 (VAP-1) was implicated in adhesion and transmigration of lymphocytes across endothelial cells in liver and other organs. There is very little information on VAP-1 expression in normal and inflamed lungs. Therefore, we conducted a study to localize VAP-1 in normal mice and human lungs and in two distinct murine models of lung inflammation. Normal mice and human lungs revealed VAP-1 expression in the endothelium of large and mid-sized pulmonary vessels but not in alveolar septae, airway epithelium or blood cells. Mice that lack the lpr −/− gene and develop extensive lymphocytic infiltration in their lungs showed VAP-1 expression similar to the normal mice lungs. Mice subjected to cecal ligation and puncture developed acute lung inflammation and showed VAP-1 not only in endothelial cells but also in inflammatory cells in perivascular areas at 72 h after the procedure. We concluded that VAP-1 expression may contribute to the functional heterogeneity of endothelial cells within the lung to create distinct sites for the recruitment of inflammatory cells. Furthermore, since VAP-1 is expressed over a longer period of time in inflamed lungs, it may even be a suitable target for drug delivery and therapeutic manipulations.

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Acknowledgements

The research was supported by a grant from Deutsche Forschungsgemeinschaft (SFB 587, B1). Dr. Baljit Singh was supported by a Study Visit Grant from the German Academic Exchange Program. The authors thank Dr. M. Salmi and Dr. S. Jalkanen for the VAP-1 antibody, and Dr. B. Imhof for the JAM-2 antibody.

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Correspondence to Baljit Singh.

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Singh, B., Tschernig, T., van Griensven, M. et al. Expression of vascular adhesion protein-1 in normal and inflamed mice lungs and normal human lungs. Virchows Arch 442, 491–495 (2003). https://doi.org/10.1007/s00428-003-0802-6

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  • DOI: https://doi.org/10.1007/s00428-003-0802-6

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