Upregulation of endothelial cell adhesion molecules characterizes veins close to granulomatous infiltrates in the renal cortex of cats with feline infectious peritonitis and is indirectly triggered by feline infectious peritonitis virus-infected monocytes in vitro

• DOI: 10.1099/jgv.0.000585
• Publication Date: 2016-08-19T15:12:28Z
• Authors: Delphine D. Acar; Dominique A. J. O...; Annelike Dedeurwa...; Inge D. M. Roukaerts; Wendy Baetens; Sebastiaan Van Bo...; Gaëtan M. A. De G...; Lowiese M. B. Des...; Hans J. Nauwynck
• Keywords: Feline infectious peritonitis

One of the most characteristic pathological changes in cats that have succumbed to feline infectious peritonitis (FIP) is a multifocal granulomatous phlebitis. Although it now well established leukocyte extravasation elicits inflammation typically associated with FIP lesions, relatively few studies aimed at elucidating this key pathogenic event. The upregulation adhesion molecules on endothelium prerequisite for stable leukocyte–endothelial cell (EC) necessarily precedes diapedesis. Therefore, present work focused expression EC and possible triggers activation during development FIP. Immunofluorescence analysis revealed endothelial P-selectin, E-selectin, intercellular molecule 1 (ICAM-1) vascular (VCAM-1) was elevated veins close infiltrates renal cortex patients compared non-infiltrated regions specimens from healthy cats. Next, we showed venous ECs become activated when exposed supernatant virus (FIPV)-infected monocytes, as indicated by increased expression. Active viral replication seemed be required induce EC-stimulating activity monocytes. Finally, assays an naive monocytes treated FIPV-infected Taken together, our results strongly indicate FIPV activates increase monocyte indirect route, which proinflammatory factors released virus-infected act intermediates.