Tumor necrosis factor-α induction by reovirus serotype 3

Farone, Anthony L.; O’Brien, Patricia C.; Çox, Donald C.

doi:10.1002/jlb.53.2.133

Cited by 20 publications

(15 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Interestingly, for TNF-αactivation was largely independent of productive infection, a finding that also indicates that induction of IL-6 and IL-10 are not being induced as a by-product of TNF-α up-regulation, but rather that these mediators are independently induced. Although the mechanism by which TNF-α induction occurs remains elusive, a similar phenomenon has been reported for a diverse range of viruses, including Ebola virus, Marburg virus, Herpes Simplex virus and Reovirus [17], [37], [38]. For Ebola virus, infection-independent TNF-α activation has been suggested to occur in response to receptor cross-linking by the viral surface glycoproteins [39] and, based on our observations, we can propose that a similar process may take place with arenavirus particles as well.…”

Section: Discussionmentioning

confidence: 57%

Tacaribe Virus but Not Junin Virus Infection Induces Cytokine Release from Primary Human Monocytes and Macrophages

et al. 2011

View full text Add to dashboard Cite

The mechanisms underlying the development of disease during arenavirus infection are poorly understood. However, common to all hemorrhagic fever diseases is the involvement of macrophages as primary target cells, suggesting that the immune response in these cells may be of paramount importance during infection. Thus, in order to identify features of the immune response that contribute to arenavirus pathogenesis, we have examined the growth kinetics and cytokine profiles of two closely related New World arenaviruses, the apathogenic Tacaribe virus (TCRV) and the hemorrhagic fever-causing Junin virus (JUNV), in primary human monocytes and macrophages. Both viruses grew robustly in VeroE6 cells; however, TCRV titres were decreased by approximately 10 fold compared to JUNV in both monocytes and macrophages. Infection of both monocytes and macrophages with TCRV also resulted in the release of high levels of IL-6, IL-10 and TNF-α, while levels of IFN-α, IFN-β and IL-12 were not affected. However, we could show that the presence of these cytokines had no direct effect on growth of either TCRV of JUNV in macrophages. Further analysis also showed that while the production of IL-6 and IL-10 are dependent on viral replication, production of TNF-α also occurs after exposure to UV-inactivated TCRV particles and is thus independent of productive virus infection. Surprisingly, JUNV infection did not have an effect on any of the cytokines examined indicating that, in contrast to other viral hemorrhagic fever viruses, macrophage-derived cytokine production is unlikely to play an active role in contributing to the cytokine dysregulation observed in JUNV infected patients. Rather, these results suggest that an early, controlled immune response by infected macrophages may be critical for the successful control of infection of apathogenic viruses and prevention of subsequent disease, including systemic cytokine dysregulation.

show abstract

Section: Discussionmentioning

confidence: 57%

Tacaribe Virus but Not Junin Virus Infection Induces Cytokine Release from Primary Human Monocytes and Macrophages

et al. 2011

View full text Add to dashboard Cite

show abstract

“…types, including macrophages, 35 fibroblasts, 34 and epithelial cells. 36 Reovirus can also induce CXCL8 production in monocytes, although in our experiments human mast cells produced 5-fold higher CXCL8 levels when infected with reovirus than reported for monocytes.…”

Section: Discussionmentioning

confidence: 99%

Human mast cell activation with virus-associated stimuli leads to the selective chemotaxis of natural killer cells by a CXCL8-dependent mechanism

Burke¹,

Issekutz

Karkada

et al. 2008

Blood

110

111

View full text Add to dashboard Cite

Human mast cells are found in skin and mucosal surfaces and next to blood vessels. They play a sentinel cell role in immunity, recognizing invading pathogens and producing proinflammatory mediators. Mast cells can recruit granulocytes, and monocytes in allergic disease and bacterial infection, but their ability to recruit antiviral effector cells such as natural killer (NK) cells and T cells has not been fully elucidated. To investigate the role of human mast cells in response to virus-associated stimuli, human cord blood-derived mast cells (CBMCs) were stimulated with polyinosinic⅐polycytidylic acid, a double-stranded RNA analog, or infected with the double-stranded RNA virus, reovirus serotype 3 Dearing for 24 hours. CBMCs responded to stimulation with polyinosinic⅐polycytidylic acid by producing a distinct chemokine profile, including CCL4, CXCL8, and CXCL10. CBMCs produced significant amounts of CXCL8 in response to low levels of reovirus infection, while both skin-and lungderived fibroblasts were unresponsive unless higher doses of reovirus were used. Supernatants from CBMCs infected with reovirus induced substantial NK cell chemotaxis that was highly dependent on CXCL8 and CXCR1. These results sug- IntroductionMast cells are long-lived resident tissue cells found close to blood vessels, and are numerous at sites in close proximity to the external environment such as the skin and airways (reviewed in Galli et al 1 and Metz and Maurer 2 ). From these strategic locations they can quickly recognize and respond to invading pathogens. They are also relatively resistant to ultraviolet (UV) and gamma irradiation. [3][4][5] Upon activation, mast cells produce a wide array of mediators, including granule-associated products, such as histamine, and preformed and de novo synthesized cytokines, chemokines, and lipid mediators. They can activate and recruit effector cells, including eosinophils, 6 neutrophils, 7 and monocytes. 8 Their role in innate immune responses to bacterial infections has been clearly delineated, however their involvement in viral infections is not well understood. Mast cells express Toll-like receptor 3 (TLR3), which recognizes viral double-stranded RNA (dsRNA), 9 and they can produce type I interferons when activated through this receptor. 10 Studies examining the permissiveness of mast cells to viruses show that they can be infected by, and respond to, dengue virus, 11,12 HIV, 13,14 and respiratory syncytial virus. 15 Human mast cells produce the chemokines CCL3, CCL4, and CCL5 when infected with dengue virus, 16 and mouse mast cells produce CCL4 and CCL5 when infected with Newcastle disease virus, all of which are known natural killer (NK) cell and T-cell chemoattractants. 17 NK cells are large granular lymphocytes that can kill virally infected cells, and are crucial for the clearance of viruses during infections (reviewed in Lodoen and Lanier 18 ). The chemokines and chemokine receptors necessary for the infiltration of NK cells into virally infected tissues have recently begun to be uncover...

show abstract

“…Hypoxia and advanced glycation endproducts (AGEs) induce TNF, IL-6 and IL-1 [154][155][156]. TNF-α increases NF-kappaB-mediated transcription [157,158] and activates PKC [159], and alters the barrier function of endothelial cells [160]. Increased levels of p55 and p75 correlate with the severity of diabetic microvascular complications, implicating raised levels of these receptors as potential markers [149,150].…”

Section: Tumor Necrosis Factor Alpha (Tnf-α) Oxidative Stress and Thmentioning

confidence: 99%

Oxidative-Nitrosative Stress as a Contributing Factor to Cardiovascular Disease in Subjects with Diabetes

Stevens¹

2005

CVP

View full text Add to dashboard Cite

In diabetes, clear evidence has emerged for the presence of oxidative-nitrosative stress, which may be a consequence of a glucose-mediated imbalance of systemic antioxidant buffering capacity, coupled with increased production of free radical species. Although multiple metabolic pathways have been identified, which may contribute to oxidative stress in diabetes, the principal pathogenetic pathways and their key down-stream targets remain to be established. Evidence links oxidative stress in particular, to elevations of postprandial glucose and lipids, which also have recently emerged as major risk factors for cardiovascular events. Indeed, considerable evidence suggests that increased oxidative stress in diabetes may play an important role in the development or progression of cardiovascular disease by a number of different mechanisms, including alterations of cardiovascular sympathetic nervous system tone and integrity, elevation of acute phase reactants, disruption of endothelial function and facilitation of myocardial injury. Despite the disappointments of recent large scale clinical trials evaluating the efficacy of antioxidants in cardiovascular disease, many therapeutic agents which have been used successfully in diabetic subjects at high risk for cardiovascular disease have a mechanism of action which includes an antioxidant capacity. Therefore, incorporating an antioxidant action in future therapeutic approaches to combat cardiovascular disease complicating diabetes, appears to remain justified and warrants further evaluation.

show abstract

Tumor necrosis factor-α induction by reovirus serotype 3

Cited by 20 publications

References 17 publications

Tacaribe Virus but Not Junin Virus Infection Induces Cytokine Release from Primary Human Monocytes and Macrophages

Tacaribe Virus but Not Junin Virus Infection Induces Cytokine Release from Primary Human Monocytes and Macrophages

Human mast cell activation with virus-associated stimuli leads to the selective chemotaxis of natural killer cells by a CXCL8-dependent mechanism

Oxidative-Nitrosative Stress as a Contributing Factor to Cardiovascular Disease in Subjects with Diabetes

Contact Info

Product

Resources

About