Measles Virus Induction of Human Endothelial Cell Tissue Factor Procoagulant Activity in Vitro

Mazure, G; Grundy, Jane E.; Nygård, G; Hudson, M; Khan, Khalid M.; Srai, K; Dhillon, AP; Pounder, RE; Wakefield, AJ

doi:10.1099/0022-1317-75-11-2863

Cited by 17 publications

(11 citation statements)

References 16 publications

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“…In our study, normal lung parenchyma was negative for TF staining of type II pneumocytes, which is consistent with the idea that TF is not normally expressed in endothelial cells or macrophages (24). A variety of stimulants, however, such as IL-1 ␤ , tumor necrosis factor-␣ (TNF-␣ ), bacterial endotoxin (25), and measles virus infection (26), have been reported to induce TF expression in these cells in vitro . Our results showing TF expression in type II pneumocytes in interstitial pneumonia, therefore, indicate that type II pneumocytes are activated under these conditions, although the precise mechanisms remain largely unknown.…”

Section: Discussionsupporting

confidence: 91%

Tissue Factor Expression and Fibrin Deposition in the Lungs of Patients with Idiopathic Pulmonary Fibrosis and Systemic Sclerosis

Imokawa

Sato²,

Hayakawa³

et al. 1997

Am J Respir Crit Care Med

145

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Although abnormalities of alveolar fibrin turnover have been reported to play a role in the development of idiopathic pulmonary fibrosis (IPF), the pathophysiological relevance remains unclear. We therefore investigated the localization of tissue factor (TF) and fibrin deposition in patients with IPF using immunohistochemistry and compared the results with those from patients who had interstitial pneumonia associated with systemic sclerosis (IP-SSc) and idiopathic bronchiolitis obliterans with organizing pneumonia (BOOP). Expression of TF-mRNA was also assessed, using in situ hybridization with a digoxigenin-labeled cRNA probe. In patients with IPF, IP-SSc, and idiopathic BOOP, the TF antigen was positively stained in type II pneumocytes and in some alveolar macrophages. The fibrin antigen was stained in the type II pneumocytes and the adjacent area. Tissue factor-mRNA was expressed in the type II pneumocytes and in some alveolar macrophages. Neither TF antigens nor TF-mRNA were detected in the normal lung. These results indicate that type II pneumocytes are a major source of TF, suggesting that TF production in these cells is closely related to fibrin deposition in the lungs of people with these diseases.

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Section: Discussionsupporting

confidence: 91%

Tissue Factor Expression and Fibrin Deposition in the Lungs of Patients with Idiopathic Pulmonary Fibrosis and Systemic Sclerosis

Imokawa

Sato²,

Hayakawa³

et al. 1997

Am J Respir Crit Care Med

145

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“…The link between MV and inflammatory bowel disease (IBD) has mainly been propagated by Andy Wakefield and his colleagues [157,158]. Although they themselves have published negative findings in relation to this link using RT/PCR [159], they considered that the ultimate sensitivity and positive proof were given in a paper by the Kawashima group [160].…”

Section: Inflammatory Bowel Diseasementioning

confidence: 99%

Morbilliviruses and human disease

Rima

Duprex

2005

The Journal of Pathology

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Morbilliviruses are a group of viruses that belong to the family Paramyxoviridae. The most instantly recognizable member is measles virus (MV) and individuals acutely infected with the virus exhibit a wide range of clinical symptoms ranging from a characteristic mild selflimiting infection to death. Canine distemper virus (CDV) and rinderpest virus (RPV) cause a similar but distinctive pathology in dogs and cattle, respectively, and these, alongside experimental MV infection of primates, have been useful models for MV pathogenesis. Traditionally, viruses were identified because a distinctive disease was observed in man or animals; an infectious agent was subsequently isolated, cultured, and this could be used to recapitulate the disease in an experimentally infected host. Thus, satisfying Koch's postulates has been the norm. More recently, particularly due to the advent of exceedingly sensitive molecular biological assays, many researchers have looked for infectious agents in disease conditions for which a viral aetiology has not been previously established. For these cases, the modified Koch's postulates of Bradford Hill have been developed as criteria to link a virus to a specific disease. Only in a few cases have these conditions been fulfilled. Therefore, many viruses have over the years been definitely and tentatively linked to human diseases and in this respect the morbilliviruses are no different. In this review, human diseases associated with morbillivirus infection have been grouped into three broad categories: (1) those which are definitely caused by the infection; (2) those which may be exacerbated or facilitated by an infection; and (3) those which currently have limited, weak, unsubstantiated or no credible scientific evidence to support any link to a morbillivirus. Thus, an attempt has been made to clarify the published data and separate human diseases actually linked to morbilliviruses from those that are merely anecdotally associated.

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“…Even in the absence of xenoreactive antibodies and C activation, xenogeneic EC injury by, for example, certain viruses with induction of procoagulant activity [85–87] and cell adhesion receptors [88,89] could have serious consequences for long‐term graft survival. These may be of greater import than in the equivalent allograft situation because of the greater potential for altered thromboregulation, altered immune defenses [90–92] and additional targeting of certain viruses to highly expressed human C regulatory proteins that bypass species‐specific cellular resistance to infection [93,94].…”

Section: Viral Mediated Procoagulant Pathwaysmentioning

confidence: 99%

Disordered regulation of coagulation and platelet activation in xenotransplantation

Robson

Cooper

d’Apice

2000

Xenotransplantation

169

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Rejection of xenografts is associated with vascular-based inflammation, thrombocytopenia and the consumption of coagulation factors that may evolve into disseminated intravascular coagulation (DIC). Similarly, bone marrow-derived cellular xenotransplantation procedures are associated with endothelial cell activation and thrombotic microangiopathic injury. These complications generally develop despite the best available measures for depletion of xenoreactive natural antibody, inhibition of complement activation and suppression of T- and B-cell mediated immune responses. The mechanisms underlying the DIC and thrombotic microangiopathy associated with xenotransplantation are unclear. A proposed primary biological dysfunction of xenografts with respect to regulation of clotting could amplify vascular injury, promote immunological responses and independently contribute to graft failure. Disordered thromboregulation could have deleterious effects, comparable to unregulated complement activation, in the pathogenesis of xenograft rejection and may therefore represent a substantive barrier to xenotransplantation.

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Measles Virus Induction of Human Endothelial Cell Tissue Factor Procoagulant Activity in Vitro

Cited by 17 publications

References 16 publications

Tissue Factor Expression and Fibrin Deposition in the Lungs of Patients with Idiopathic Pulmonary Fibrosis and Systemic Sclerosis

Tissue Factor Expression and Fibrin Deposition in the Lungs of Patients with Idiopathic Pulmonary Fibrosis and Systemic Sclerosis

Morbilliviruses and human disease

Disordered regulation of coagulation and platelet activation in xenotransplantation

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