title: Potential role of proinflammatory cytokines in the pathogenetic mechanisms of vascular lesions in goats naturally infected with bluetongue virus serotype 1.
abstract: 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.
authors.affiliation: Department of Comparative Pathology, Veterinary Faculty, University of Córdoba-Agrifood Excellence International Campus (ceiA3), Córdoba, Spain. an2sacop@uco.es
authors.forename: P J
authors.initials: PJ
authors.lastname: Sánchez-Cordón
authors.forename: M
authors.initials: M
authors.lastname: Pedrera
authors.forename: M A
authors.initials: MA
authors.lastname: Risalde
authors.forename: V
authors.initials: V
authors.lastname: Molina
authors.forename: B
authors.initials: B
authors.lastname: Rodríguez-Sánchez
authors.forename: A
authors.initials: A
authors.lastname: Núñez
authors.forename: J M
authors.initials: JM
authors.lastname: Sánchez-Vizcaíno
authors.forename: J C
authors.initials: JC
authors.lastname: Gómez-Villamandos
mesh_terms: D000818:Animals; D001819:Bluetongue / Q000150:complications / Q000276:immunology* / Q000473:pathology; D001820:Bluetongue virus / Q000235:genetics / Q000472:pathogenicity*; D002463:Cell Membrane Permeability; D004487:Edema / Q000209:etiology / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D006041:Goats; D006470:Hemorrhage / Q000209:etiology / Q000378:metabolism; D007124:Immunoenzyme Techniques; D018836:Inflammation Mediators / Q000378:metabolism; D053582:Interleukin-1alpha / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics; D012367:RNA, Viral / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism*; D014652:Vascular Diseases / Q000276:immunology / Q000473:pathology* / Q000821:virology
chemical_list: D018836:Inflammation Mediators; D053582:Interleukin-1alpha; D012333:RNA, Messenger; D012367:RNA, Viral; D014409:Tumor Necrosis Factor-alpha