Promotion of IL8, IL10, TNFα and TNFβ production by EBV infection

Klein, Sigrid; Kube, Dieter; Abts, Harry F.; Diehl, Volker; Tesch, Hans

doi:10.1016/0145-2126(96)00029-x

Cited by 59 publications

(54 citation statements)

References 15 publications

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“…After incubation of cells with brefeldin A, which prevents cytokine secretion by allowing its accumulation in the cytoplasm, and intracytoplasmic labelling, synthesis of cytokines was estimated by¯ow cytometry (Picker et al, 1995). As expected (Klein et al, 1996), we have found highest levels of IL10 in LCL cells and intermediate levels of IL10 in Burkitt EBV(+) cells (Figure 2). Intracytoplasmic levels of IL10 were similar in IkBa transfected cells and non transfected cells (Figure 2).…”

Section: Phenotypic Analysis Of Ikba Transfected Clonessupporting

confidence: 87%

Relationship between IκBα constitutive expression, TNFα synthesis, and apoptosis in EBV-infected lymphoblastoid cells

et al. 1998

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In order to understand the role of NF-kB in EBV transformation we have established stably transfected IkBa into lymphoblastoid cells. Two clones were obtained in which the loss of NF-kB binding activity correlated with the constitutive expression of the transgenic IkBa. Protein latency expression was determined by immunocytochemistry. Expression of surface markers, intracytoplasmic content of cytokines cell cycle analysis after BrdU incorporation and DNA staining with propidium iodide were studied by¯ow cytometry. Percentage of apoptotic cells was determined by in-situ labelling of DNA strand breaks. No signi®cative changes in EBV latency nor in cell surface marker expression was found. In contrast, intracytoplasmic TNFa levels were strongly reduced in transfected clones. Furthermore, 30% of IkBa transfected cells were apoptotic after 8 h of TNFa treatment. This correlated with a strong reduction of BrdU incorporation after 24 h of TNFa treatment. No e ect was seen with non transfected cells or with cells transfected with a control plasmid. Our results suggest that the TNFa gene could be one of the targets of NF-kB in EBV infected cells and that NF-kB protects EBV-infected cells from apoptosis induced by TNFa, which may favour the proliferative e ect of this cytokine.

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Section: Phenotypic Analysis Of Ikba Transfected Clonessupporting

confidence: 87%

Relationship between IκBα constitutive expression, TNFα synthesis, and apoptosis in EBV-infected lymphoblastoid cells

et al. 1998

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“…2 It has been shown that in contrast to normal hematopoietic cells, in EBV-immortalized B cells, EBV-positive Burkitt's lymphoma (BL) cells and in CD40 stimulated B cells, IL-10 is expressed. 6,[13][14][15][16] However, the mechanism of the IL-10 induction in B cells is still unclear. 15,17,18 IL-10 induction by stimulation of human blood cultures with bacterial lipopolysaccharide (LPS) was found to be TNF and cAMP-dependent and shows large interindividual variations.…”

Section: Introductionmentioning

confidence: 99%

“…6,[13][14][15][16] However, the mechanism of the IL-10 induction in B cells is still unclear. 15,17,18 IL-10 induction by stimulation of human blood cultures with bacterial lipopolysaccharide (LPS) was found to be TNF and cAMP-dependent and shows large interindividual variations. [19][20][21] The haplotype IL-10.R2/IL10.G14 was associated with highest IL-10 secretion overall, whereas the haplotype IL10.R3/IL10.G7 was associated with lowest IL-10 secretion.…”

Section: Introductionmentioning

confidence: 99%

“…19,[21][22][23][24] In EBV-positive BL cell lines, IL-10 is constitutively expressed at high levels. 14,15,17,25 In contrast, most EBV-negative BL cell lines do not express IL-10. [14][15][16]25 The infection of normal B cells with EBV leads to an immortalization of these cells and the expression of IL-10 in vitro.…”

Section: Introductionmentioning

confidence: 99%

“…14,15,17,25 In contrast, most EBV-negative BL cell lines do not express IL-10. [14][15][16]25 The infection of normal B cells with EBV leads to an immortalization of these cells and the expression of IL-10 in vitro. 13 EBV, a ␥-herpesvirus, is detectable in a number of tumours including BL, Hodgkin's disease and nasopharyngeal carcinomas.…”

Section: Introductionmentioning

confidence: 99%

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The AT-rich region between −54 to −66 is important for the promoter activity of interleukin-10 in Epstein–Barr virus positive Burkitt’s lymphoma cells

et al. 1999

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IL-10 is an important regulatory cytokine. The recent characterization of the 5Ј-flanking region of IL-10 led to the identification of the promoter region. The infection of B cells with EBV induces IL-10 production which may contribute to EBV-induced transformation. In the present report, IL-10 promoter elements involved in the constitutive expression of IL-10 in EBV-positive lymphoma cells are described. The AT-rich region between −54/−66 from the transcriptional start site was found to be important for IL-10-promoter activity in BL36. A point mutation at position −60 (T/A) was associated with over 90% reduction of luciferase activity in the cell lines BL36 and BL74. The conversion of A/T at position −57 led to enhanced promoter activity. In addition the AT-rich region could serve as an enhancer for the ␤-globin basic promoter. In BJAB cells (EBV-negative), sequences between −205/−139 rather than the AT-rich region were involved in IL-10 promoter regulation. This underlines the importance of the AT-rich region for EBV-associated IL-10 promoter regulation. Our results further the understanding of how the IL-10 gene could be regulated in B cell lymphomas.

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To binge or not to binge: Binge drinking disrupts glucose homeostasis by impairing hypothalamic but not liver insulin signaling

Garcı́a-Ruiz

Fernández-Checa

2013

Hepatology

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Individuals with a history of binge drinking have an increased risk of developing the metabolic syndrome and type 2 diabetes. Whether binge drinking impairs glucose homeostasis and insulin action is unknown. To test this, we treated Sprague-Dawley rats daily with alcohol (3 g/kg) for three consecutive days to simulate human binge drinking and found that these rats developed and exhibited insulin resistance even after blood alcohol concentrations had become undetectable. The animals were resistant to insulin for up to 54 hours after the last dose of ethanol, chiefly a result of impaired hepatic and adipose tissue insulin action. Because insulin regulates hepatic glucose production and white adipose tissue lipolysis, in part through signaling in the central nervous system, we tested whether binge drinking impaired brain control of nutrient partitioning. Rats that had consumed alcohol exhibited impaired hypothalamic insulin action, defined as the ability of insulin infused into the mediobasal hypothalamus to suppress hepatic glucose production and white adipose tissue lipolysis. Insulin signaling in the hypothalamus, as assessed by insulin receptor and AKT phosphorylation, decreased after binge drinking. Quantitative polymerase chain reaction showed increased hypothalamic inflammation and expression of protein tyrosine phosphatase 1B (PTP1B), a negative regulator of insulin signaling. Intracerebroventricular infusion of CPT-157633, a small-molecule inhibitor of PTP1B, prevented binge drinking-induced glucose intolerance. These results show that, in rats, binge drinking induces systemic insulin resistance by impairing hypothalamic insulin action and that this effect can be prevented by inhibition of brain PTP1B.

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Promotion of IL8, IL10, TNFα and TNFβ production by EBV infection

Cited by 59 publications

References 15 publications

Relationship between IκBα constitutive expression, TNFα synthesis, and apoptosis in EBV-infected lymphoblastoid cells

Relationship between IκBα constitutive expression, TNFα synthesis, and apoptosis in EBV-infected lymphoblastoid cells

The AT-rich region between −54 to −66 is important for the promoter activity of interleukin-10 in Epstein–Barr virus positive Burkitt’s lymphoma cells

To binge or not to binge: Binge drinking disrupts glucose homeostasis by impairing hypothalamic but not liver insulin signaling

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