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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

(2016) JOURNAL OF GENERAL VIROLOGY. 97(10). p.2633-2642
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Abstract
One of the most characteristic pathological changes in cats that have succumbed to feline infectious peritonitis (FIP) is a multifocal granulomatous phlebitis. Although it is now well established that leukocyte extravasation elicits the inflammation typically associated with FIP lesions, relatively few studies have aimed at elucidating this key pathogenic event. The upregulation of adhesion molecules on the endothelium is a prerequisite for stable leukocyte-endothelial cell (EC) adhesion that necessarily precedes leukocyte diapedesis. Therefore, the present work focused on the expression of the EC adhesion molecules and possible triggers of EC activation during the development of FIP. Immunofluorescence analysis revealed that the endothelial expression of P-selectin, E-selectin, intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) was elevated in veins close to granulomatous infiltrates in the renal cortex of FIP patients compared to non-infiltrated regions and specimens from healthy cats. Next, we showed that feline venous ECs become activated when exposed to supernatant from feline infectious peritonitis virus (FIPV)-infected monocytes, as indicated by increased adhesion molecule expression. Active viral replication seemed to be required to induce the EC-stimulating activity in monocytes. Finally, adhesion assays revealed an increased adhesion of naive monocytes to ECs treated with supernatant from FIPV-infected monocytes. Taken together, our results strongly indicate that FIPV activates ECs to increase monocyte adhesion by an indirect route, in which proinflammatory factors released from virus-infected monocytes act as key intermediates.
Keywords
INFLAMMATORY RESPONSE, VASCULAR ENDOTHELIUM, CORONAVIRUS, EXPRESSION, MECHANISMS, LEUKOCYTES, SELECTINS, PROTEIN, VIVO

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MLA
Acar, Delphine et al. “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.” JOURNAL OF GENERAL VIROLOGY 97.10 (2016): 2633–2642. Print.
APA
Acar, D., Olyslaegers, D., Dedeurwaerder, A., Roukaerts, I., Baetens, W., Van Bockstael, S., De Gryse, G., et al. (2016). 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. JOURNAL OF GENERAL VIROLOGY, 97(10), 2633–2642.
Chicago author-date
Acar, Delphine, Dominique Olyslaegers, Annelike Dedeurwaerder, Inge Roukaerts, Wendy Baetens, Sebastiaan Van Bockstael, Gaëtan De Gryse, Lowiese Desmarets, and Hans Nauwynck. 2016. “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.” Journal of General Virology 97 (10): 2633–2642.
Chicago author-date (all authors)
Acar, Delphine, Dominique Olyslaegers, Annelike Dedeurwaerder, Inge Roukaerts, Wendy Baetens, Sebastiaan Van Bockstael, Gaëtan De Gryse, Lowiese Desmarets, and Hans Nauwynck. 2016. “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.” Journal of General Virology 97 (10): 2633–2642.
Vancouver
1.
Acar D, Olyslaegers D, Dedeurwaerder A, Roukaerts I, Baetens W, Van Bockstael S, et al. 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. JOURNAL OF GENERAL VIROLOGY. 2016;97(10):2633–42.
IEEE
[1]
D. Acar et al., “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,” JOURNAL OF GENERAL VIROLOGY, vol. 97, no. 10, pp. 2633–2642, 2016.
@article{8504580,
  abstract     = {{One of the most characteristic pathological changes in cats that have succumbed to feline infectious peritonitis (FIP) is a multifocal granulomatous phlebitis. Although it is now well established that leukocyte extravasation elicits the inflammation typically associated with FIP lesions, relatively few studies have aimed at elucidating this key pathogenic event. The upregulation of adhesion molecules on the endothelium is a prerequisite for stable leukocyte-endothelial cell (EC) adhesion that necessarily precedes leukocyte diapedesis. Therefore, the present work focused on the expression of the EC adhesion molecules and possible triggers of EC activation during the development of FIP. Immunofluorescence analysis revealed that the endothelial expression of P-selectin, E-selectin, intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) was elevated in veins close to granulomatous infiltrates in the renal cortex of FIP patients compared to non-infiltrated regions and specimens from healthy cats. Next, we showed that feline venous ECs become activated when exposed to supernatant from feline infectious peritonitis virus (FIPV)-infected monocytes, as indicated by increased adhesion molecule expression. Active viral replication seemed to be required to induce the EC-stimulating activity in monocytes. Finally, adhesion assays revealed an increased adhesion of naive monocytes to ECs treated with supernatant from FIPV-infected monocytes. Taken together, our results strongly indicate that FIPV activates ECs to increase monocyte adhesion by an indirect route, in which proinflammatory factors released from virus-infected monocytes act as key intermediates.}},
  author       = {{Acar, Delphine and Olyslaegers, Dominique and Dedeurwaerder, Annelike and Roukaerts, Inge and Baetens, Wendy and Van Bockstael, Sebastiaan and De Gryse, Gaëtan and Desmarets, Lowiese and Nauwynck, Hans}},
  issn         = {{0022-1317}},
  journal      = {{JOURNAL OF GENERAL VIROLOGY}},
  keywords     = {{INFLAMMATORY RESPONSE,VASCULAR ENDOTHELIUM,CORONAVIRUS,EXPRESSION,MECHANISMS,LEUKOCYTES,SELECTINS,PROTEIN,VIVO}},
  language     = {{eng}},
  number       = {{10}},
  pages        = {{2633--2642}},
  title        = {{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}},
  url          = {{http://dx.doi.org/10.1099/jgv.0.000585}},
  volume       = {{97}},
  year         = {{2016}},
}

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