Proinflammatory factors present in sera from patients with acute dengue infection induce activation and apoptosis of human microvascular endothelial cells: Possible role of TNF-α in endothelial cell damage in dengue

Cardier, José E.; Mariño, Eliana; Romano, Egidio; Taylor, Peter; Liprandi, Ferdinando; Bosch, Norma B. de; Rothman, Alan L.

doi:10.1016/j.cyto.2005.01.021

Cited by 100 publications

(72 citation statements)

References 17 publications

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“…6). A similar result has been observed for other viruses causing VHFs, where neutralization of TNF-␣ released from infected monocytes or present in patient sera inhibits endothelial activation and permeability (1,8,17). Although ECs are activated upon infection, as shown by our study, the indirect targeting by moDCs is also an important mediator of endothelial activation.…”

Section: Fig 2 Activation Of Endothelial Cells Is Virus Dose Dependsupporting

confidence: 63%

“…Previously, studies have focused on the indirect role of the endothelium, since CCHFV infects dendritic cells and macrophages (11,30) and soluble mediators from CCHFV-infected dendritic cells activated ECs (30). Further support for an indirect effect of ECs for other VHFs comes from the identification of tumor necrosis factor alpha (TNF-␣) as a key mediator of endothelial cell activation (1,8,17). A direct effect on ECs was recently shown by hantaviruses, with loss of barrier integrity followed by increased permeability due to internalization of vascular endothelial (VE) cadherin (35), an important component of adherens junctions (40,44).…”

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confidence: 99%

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Crimean-Congo Hemorrhagic Fever Virus Activates Endothelial Cells

Connolly‐Andersen

Moll

Andersson

et al. 2011

J Virol

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Crimean-Congo hemorrhagic fever virus (CCHFV) causes viral hemorrhagic fever with high case-fatality rates and is geographically widely distributed. Due to the requirement for a biosafety level 4 (BSL-4) laboratory and the lack of an animal model, knowledge of the viral pathogenesis is limited. Crimean-Congo hemorrhagic fever (CCHF) is characterized by hemorrhage and vascular permeability, indicating the involvement of endothelial cells (ECs). The interplay between ECs and CCHFV is therefore important for understanding the pathogenesis of CCHF. In a previous study, we found that CCHFV-infected monocyte-derived dendritic cells (moDCs) activated ECs; however, the direct effect of CCHFV on ECs was not investigated. Here, we report that ECs are activated upon infection, as demonstrated by upregulation of mRNA levels for E-selectin, vascular cell adhesion molecule 1 (VCAM1), and intercellular adhesion molecule 1 (ICAM1). Protein levels and cell surface expression of ICAM1 responded in a dose-dependent manner to increasing CCHFV titers with concomitant increase in leukocyte adhesion. Furthermore, we examined vascular endothelial (VE) cadherin in CCHFVinfected ECs by different approaches. Infected ECs released higher levels of interleukin 6 (IL-6) and IL-8; however, stimulation of resting ECs with supernatants derived from infected ECs did not result in increased ICAM1 expression. Interestingly, the moDC-mediated activation of ECs was abrogated by addition of neutralizing tumor necrosis factor alpha (TNF-␣) antibody to moDC supernatants, thereby identifying this soluble mediator as the key cytokine causing EC activation. We conclude that CCHFV can exert both direct and indirect effects on ECs.

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Section: Fig 2 Activation Of Endothelial Cells Is Virus Dose Dependsupporting

confidence: 63%

mentioning

confidence: 99%

Crimean-Congo Hemorrhagic Fever Virus Activates Endothelial Cells

Connolly‐Andersen

Moll

Andersson

et al. 2011

J Virol

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“…Among them are a rapid and uncontrolled increase in the levels of cytokines, especially TNF-α and IFN-γ, which in turn induce the clinical manifestations of DHF such as plasma leakage, shock, and hemorrhagic manifestations. [27][28][29] In the present study, we examined the memory cellular immune response by measuring the expression of two critical mediators of pro-inflammatory response (IFN-γ and TNF-α) and two central mediators of regulatory response (TGF-β and IL-10). 24 Our results show that TNF-α and IFN-γ mRNA expression was significantly lower in the dengue-naive control group compared with all dengue-immune persons (P 0.001).…”

Section: Discussionmentioning

confidence: 99%

Variation in Inflammatory/Regulatory Cytokines in Secondary, Tertiary, and Quaternary Challenges with Dengue Virus

Sierra

Pérez²,

Álvarez³

et al. 2012

The American Society of Tropical Medicine and Hygiene

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Abstract. Secondary heterologous dengue infection is a risk factor for severe disease manifestations because of the immune-enhancement phenomenon. Succeeding clinical infections are seldom reported, and the clinical course of tertiary and quaternary dengue infections is not clear. Cuba represents a unique environment to study tertiary/quaternary dengue infections in a population with known clinical and serologic dengue markers and no dengue endemicity. We took advantage of this exceptional epidemiologic condition to study the effect of primary, secondary, tertiary, and quaternary dengue infection exposure on the expression of pro-inflammatory and regulatory cytokines, critical in dengue infection pathogenesis, by using a dengue infection ex vivo model. Whereas secondary exposure induced a high cytokine response, we found a significantly lower expression of tumor necrosis factor-α, interferon-γ, interleukin-10, and tumor growth factor-β after tertiary and quaternary infectious challenge. Significant differences in expression of the cytokines were seen between the dengue immune profiles, suggesting that the sequence in which the immune system encounters serotypes may be important in determining the nature of the immune response to subsequent infections.

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“…All patients were enrolled in a study protocol conducted by the University of Massachusetts Medical School (UMMS), Worcester, MA, USA and Banco Municipal de Sangre del Distrito Capital (BMS), Caracas, Venezuela, between 2001 and 2005 [55]. Written informed consent was obtained from all subjects.…”

Section: Patientsmentioning

confidence: 99%

Elevated levels of soluble ST2 protein in dengue virus infected patients

et al. 2008

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Levels of the soluble form of the interleukin-1 receptor like 1 protein (IL-1RL-1 / ST2) are elevated in the serum of patients with diseases characterized by an inflammatory response. The objective of this study was to determine the concentration of soluble ST2 (sST2) in dengue infected patients during the course of the disease. Twenty four patients with confirmed dengue infection, classified as dengue fever, and eleven patients with other febrile illness (OFI) were evaluated. Levels of sST2 in serum and laboratory variables usually altered during dengue infections were measured. Dengue infected patients had higher serum sST2 levels than OFI at the end of the febrile stage and at defervescence (p=0.0088 and p=0.0004 respectively). Patients with secondary dengue infections had higher serum sST2 levels compared with patients with primary dengue infections (p=0.047 at last day of fever and p=0.030 at defervescence). Furthermore, in dengue infected patients, we found a significant negative correlation of sST2 with platelet and WBC counts, and positive correlation with thrombin time and transaminases activity. We suggest that sST2 could be a potential marker of dengue infection, could be associated with severity or could play a role in the immune response in secondary dengue virus infection.

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Proinflammatory factors present in sera from patients with acute dengue infection induce activation and apoptosis of human microvascular endothelial cells: Possible role of TNF-α in endothelial cell damage in dengue

Cited by 100 publications

References 17 publications

Crimean-Congo Hemorrhagic Fever Virus Activates Endothelial Cells

Crimean-Congo Hemorrhagic Fever Virus Activates Endothelial Cells

Variation in Inflammatory/Regulatory Cytokines in Secondary, Tertiary, and Quaternary Challenges with Dengue Virus

Elevated levels of soluble ST2 protein in dengue virus infected patients

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