Cytomegalovirus‐Infected Endothelial Cells Recruit Neutrophils by the Secretion of C‐X‐C Chemokines and Transmit Virus by Direct Neutrophil‐Endothelial Cell Contact and during Neutrophil Transendothelial Migration

Grundy, Jane E.; Lawson, Keirissa; MacCormac, Luci P.; Fletcher, Jean M.; Yong, Kwee

doi:10.1086/515300

Cited by 182 publications

(177 citation statements)

References 25 publications

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“…Other factors such as cytokine dysregulation induced by herpesvirus reactivation may have effects on HCV recurrence. Both CMV and HHV-6 infection have been associated with the up-regulation of several cytokines (16)(17)(18). For example, HHV-6 infection results in the potent induction of tumor necrosis factor-a, which is thought to play important role in the pathogenesis of HCV (16,19).…”

Section: Discussionmentioning

confidence: 99%

Interactions Between Cytomegalovirus, Human Herpesvirus‐6, and the Recurrence of Hepatitis C After Liver Transplantation

Humar

Kumar

Raboud

et al. 2002

American Journal of Transplantation

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Recurrence of hepatitis C (HCV) following liver transplantation is common. Herpesvirus reactivation following transplant may have an immunomodulatory effect resulting in increased HCV replication. We studied whether cytomegalovirus (CMV) and human herpesvirus-6 (HHV-6) may be associated with HCV recurrence and viral load after transplant. We prospectively followed 66 HCV liver-transplant recipients with serial viral load testing for CMV and HHV-6. Infection and viral load were correlated with the development of biopsy-proven HCV recurrence and HCV viral loads. Histologic recurrence of HCV occurred in 41/66 (62.1%) patients. In the primary analysis, CMV infection and disease, and HHV-6 infection were not associated with HCV recurrence. Peak CMV and HHV-6 viral loads were not significantly different in patients with and without recurrence. No correlation was observed between HCV viral loads at 1 and 3 months post-transplant and peak HHV-6 or CMV viral loads. In a subgroup analysis, HHV-6 infection was associated with the development of more severe recurrence (hepatitis and/or fibrosis score Ն2) (p Ω 0.01). Also, fibrosis scores at last follow up were higher in patients with CMV disease (1.67 vs. 0.56; p Ω 0.016) and in patients with HHV-6 infection (1.18 vs. 0.55; p Ω 0.031). In conclusion, HHV-6 and CMV infection and viral load were not associated with increased overall rates of HCV recurrence or HCV viral load after liver transplantation but may be associated with more severe forms of recurrence.

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Section: Discussionmentioning

confidence: 99%

Interactions Between Cytomegalovirus, Human Herpesvirus‐6, and the Recurrence of Hepatitis C After Liver Transplantation

Humar

Kumar

Raboud

et al. 2002

American Journal of Transplantation

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“…In contrast, HCMV may contribute to pathogenesis due to altered cellular gene expression that occurs independent of virus replication. For example, HCMV has been shown to alter the expression of cellular genes that code for proteins with proinflammatory activity, including adhesion molecules (1,2), chemokines (3)(4)(5)(6)(7), and extracellular matrix proteins (8 -10). HCMV may contribute to inflammatory mechanisms by modulation of multiple constituents of the PG synthesis pathway via arachidonic acid.…”

Section: H Uman CMV (Hcmv)mentioning

confidence: 99%

Human Cytomegalovirus Circumvents NF-κB Dependence in Retinal Pigment Epithelial Cells

Činátl¹,

Margraf²,

Vogel³

et al. 2001

The Journal of Immunology

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The human CMV (HCMV) is a persistent virus that may cause severe inflammatory responses especially in immunocompromised hosts. In different cell types, HCMV infection leads to the activation of the pleiotropic transcription factor, NF-κB, which triggers virus replication but also propagates cell-mediated inflammatory mechanisms that largely depend on PG synthesis. We investigated the interactions of HCMV and the NF-κB-dependent PG synthesis pathway in cultures of retinal pigment epithelial (RPE) cells that are known to be infected in HCMV retinitis patients. Unlike in other cell types, HCMV increased neither NF-κB activity nor p65 and p105/50 mRNA levels in RPE cells. Both TNF-α and phorbol ester 12,0-tetradecanoylphorbol 13-acetate (TPA) enhanced NF-κB activity but only TPA increased HCMV replication. Cyclooxygenase-2 expression and PGE2 release was increased by TPA and TNF-α but not by HCMV infection. Stimulatory activity of TPA on HCMV replication was suppressed by protein kinase C inhibitors and inhibitors of p42/44 and p38 mitogen-activated protein kinases but not by NF-κB inhibitors. In conclusion, HCMV circumvents the NF-κB route in favor of the protein kinase C-dependent mitogen-activated protein kinase pathway in RPE cells. This virus/host cell interaction might be a mechanism that promotes HCMV persistence in immune-privileged organs such as the eye.

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“…18 Bacterial and viral infections induce proinflammatory activation of the vascular endothelium, which leads to adherence/sequestration of PMNs. 21,[36][37][38][39] Other first events have been implicated, including cytokine administration, massive transfusion, recent surgery (especially cardiovascular surgery), and induction chemotherapy, but only infections have been studied to date in vivo. 2,18,27,[40][41][42][43][44] PMNs were also required because granulocyte depletion inhibited ALI.…”

mentioning

confidence: 99%

Plasma from stored packed red blood cells and MHC class I antibodies causes acute lung injury in a 2-event in vivo rat model

Kelher

Masuno

Moore

et al. 2009

Blood

141

276

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Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion death. We hypothesize that TRALI requires 2 events: (1) the clinical condition of the patient and (2) the infusion of antibodies against MHC class I antigens or the plasma from stored blood. A 2-event rat model was developed with saline (NS) or endotoxin (LPS) as the first event and the infusion of plasma from packed red blood cells (PRBCs) or antibodies (OX18 and OX27) against MHC class I antigens as the second event. ALI was determined by Evans blue dye leak from the plasma to the bronchoalveolar lavage fluid (BALF), protein and CINC-1 concentrations in the BALF, and the lung histology. NS-treated rats did not evidence ALI with any second events, and LPS did not cause ALI. LPS-treated animals demonstrated ALI in response to plasma from stored PRBCs, both prestorage leukoreduced and unmodified, and to OX18 and OX27, all in a concentration-dependent fashion. ALI was neutrophil (PMN) dependent, and OX18/OX27 localized to the PMN surface in vivo and primed the oxidase of rat PMNs. We conclude that TRALI is the result of 2 events with the second events consisting of the plasma from stored blood and antibodies that prime PMNs. IntroductionTransfusion-related acute lung injury (TRALI) is the leading cause of transfusion mortality in the United States. 1,2 TRALI is the acute onset of noncardiogenic pulmonary edema as documented by chest radiograph and profound hypoxemia, in accordance with the definition of acute lung injury (ALI), that occurs within 6 hours of transfusion. 3,4 TRALI may occur with or without conditions that predispose the patient to ALI, and may be the worsening of pulmonary function in patients with preexisting ALI. 3,4 All blood products have been implicated in TRALI, but components that contain large amounts of plasma are mainly responsible. 5,6 The current incidence of TRALI has been estimated as 1/7900 to 1/1330 in the United Kingdom and the United States with lesser incidences in Europe. [5][6][7][8] Current mortality rates vary from 5% to 35% with the lesser mortality rates predominating. [5][6][7][8] The pathophysiology of TRALI has not been elucidated despite numerous studies. [9][10][11][12][13][14] The first mechanism proposed was the infusion of donor antibodies directed against the HLA class I or granulocyte-specific antigens on the recipient's leukocytes with animal models composed of an in vivo murine model and an isolated, perfused rabbit lung that provided physiologic relevance. [9][10][11][12]14 In addition, the neutrophil (PMN) was proposed to be the effector cell, identical to other forms of ALI and the acute respiratory distress syndrome (ARDS). [9][10][11][12]14 However, look-back studies of donors with specific antibodies directed against HLA or granulocyte antigens demonstrated that the infusion of donor antibodies into a recipient that expressed the cognate antigen resulted in TRALI in a minority of these patients, implying that the clinical condition of the recipient may be important for the d...

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Cytomegalovirus‐Infected Endothelial Cells Recruit Neutrophils by the Secretion of C‐X‐C Chemokines and Transmit Virus by Direct Neutrophil‐Endothelial Cell Contact and during Neutrophil Transendothelial Migration

Cited by 182 publications

References 25 publications

Interactions Between Cytomegalovirus, Human Herpesvirus‐6, and the Recurrence of Hepatitis C After Liver Transplantation

Interactions Between Cytomegalovirus, Human Herpesvirus‐6, and the Recurrence of Hepatitis C After Liver Transplantation

Human Cytomegalovirus Circumvents NF-κB Dependence in Retinal Pigment Epithelial Cells

Plasma from stored packed red blood cells and MHC class I antibodies causes acute lung injury in a 2-event in vivo rat model

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