Present address: Department of Clinical Microbiology and Infectious Diseases, Universitary General Hospital ‘Gregorio Marañón’, Madrid, Spain.
Potential Role of Proinflammatory Cytokines in the Pathogenetic Mechanisms of Vascular Lesions in Goats Naturally Infected with Bluetongue Virus Serotype 1
Version of Record online: 20 MAY 2012
© Her Majesty the Queen in Right of Canada 2012. Reproduced with the permission of the Minister of Canadian Food Inspection Agency
Transboundary and Emerging Diseases
Volume 60, Issue 3, pages 252–262, June 2013
How to Cite
Sánchez-Cordón, P. J., Pedrera, M., Risalde, M. A., Molina, V., Rodríguez-Sánchez, B., Núñez, A., Sánchez-Vizcaíno, J. M. and Gómez-Villamandos, J. C. (2013), Potential Role of Proinflammatory Cytokines in the Pathogenetic Mechanisms of Vascular Lesions in Goats Naturally Infected with Bluetongue Virus Serotype 1. Transboundary and Emerging Diseases, 60: 252–262. doi: 10.1111/j.1865-1682.2012.01343.x
Reproduced with the permission of the Controller of Her Majesty's Stationery Office/Queen's Printer for Scotland and Animal Health and Veterinary Laboratories Agency.
- Issue online: 15 APR 2013
- Version of Record online: 20 MAY 2012
- Received for publication February 20, 2012
- bluetongue virus;
- vascular lesions;
In vitro studies have demonstrated that bluetongue virus (BTV)-induced vasoactive mediators could contribute to the endothelial cells dysfunction and increased vascular permeability responsible of lesions characteristic of bluetongue (BT) like oedema, haemorrhages and ischaemic necrosis in different tissues. However, few in vivo studies have been carried out to clarify the causes of these lesions. The aim of this study was to elucidate in vivo the pathogenetic mechanisms involved in the appearance of vascular lesions in different organs during BT. For this purpose, tissue samples from goats naturally infected with bluetongue virus serotype 1 (BTV-1) were taken for histopathological and immunohistochemical studies to determine the potential role of proinflammatory cytokines (tumour necrosis factor alpha, TNFα and interleukin one alpha, IL-1α) in the increased vascular permeability and their relationship with the presence of virus. Gross and histopathological examination revealed the presence of vascular damage leading to generalized oedema and haemorrhages. Immunohistochemical studies displayed that endothelial injury may have been due to the direct pathogenic effect of BTV infection on endothelial cells or may be a response to inflammatory mediators released by virus-infected endothelial cells and, possibly, other cell types such as monocytes/macrophages. These preliminary results of what appears to be the first in vivo study of tissue damage in small BT-infected ruminants suggest a direct link between the appearance of vascular changes and the presence of BTV-induced vasoactive cytokines.