Home \ Research \ Scientific publications \


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 publish this investigation article

June 1st, 2013

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




Sanchez-Cordon PJ., Pedrera M., Risalde MA., Molina V., Rodriguez B., Nunez A., Sanchez-Vizcaino JM. and Gomez-Villamandos JC.




See this article
Potential role of proinflammatory cytokines in the pathogenetic mechanisms of vascular lesions in goats naturally infected with Bluetongue virus Serotype 1

See it on NLM PubMed
Potential role of proinflammatory cytokines in the pathogenetic mechanisms of vascular lesions in goats naturally infected with Bluetongue virus Serotype 1



Participants:

Universidad ComplutenseServicio de Inmunología Viral y Medicina Preventiva (SUAT). Centro de Vigilancia Sanitaria Veterinaria (VISAVET). Universidad Complutense (UCM).

Universidad ComplutenseDepartamento de Sanidad Animal. Facultad de Veterinaria. Universidad Complutense (UCM).

Universidad de CórdobaDepartamento de Anatomía y Anatomía Patológica Comparadas. Facultad de Veterinaria. Universidad de Córdoba (UCO).

Department for Environment, Food and Rural AffairsDepartment of Pathology and Host Susceptibility. Department for Bovine Tuberculosis. Animal Health and Veterinary Laboratories Agency (AHVLA). Department for Environment, Food and Rural Affairs (Defra).







Transboundary and Emerging Diseases
FACTOR YEAR Q
3.116 2013

NLMID: 101319538

PMID: 22607118

ISSN: 1865-1674



TITLE: Potential role of proinflammatory cytokines in the pathogenetic mechanisms of vascular lesions in goats naturally infected with Bluetongue virus Serotype 1


JOURNAL: Transbound. Emerg. Dis.


NUMERACIÓN: 60(3):252-62


AÑO: 2013


PUBLISHER: Blackwell Verlag


AUTHORS: Sanchez-Cordon PJ., Pedrera M., Risalde MA., Molina V., Rodriguez B., Nunez A., Sanchez-Vizcaino JM. and Gomez-Villamandos JC.


VISAVET PARTICIPANTS


José Manuel Sánchez-Vizcaíno Rodríguez

DOI: https://doi.org/ 10.1111/j.1865-1682.2012.01343.x


CITE THIS PUBLICATION:

Sanchez-Cordon PJ., Pedrera M., Risalde MA., Molina V., Rodriguez B., Nunez A., Sanchez-Vizcaino JM. and Gomez-Villamandos JC. 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(3):252-62. 2013. (A). ISSN: 1865-1674. DOI: 10.1111/j.1865-1682.2012.01343.x


UNITS: