Epstein-Barr virus modulates de novo protein synthesis in human neutrophils

Beaulieu, André; Paquin, Robert; Gosselin, Jean

doi:10.1182/blood.v86.7.2789.2789

Cited by 16 publications

(6 citation statements)

References 34 publications

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“…Cells infected with purified virus were cultured in MEM supplemented with 5% heat-inactivated FBS until 90% of mortality was observed. Supernatant was then filtered on 0.45 µm pore filter and viral particles were concentrated by ultracentrifugation [37] . Uninfected-BHK-21 cells supernatant was treated as above to produce mock control.…”

Section: Methodsmentioning

confidence: 99%

Involvement of TLR2 in Recognition of Acute Gammaherpesvirus-68 Infection

et al. 2010

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BackgroundToll-like receptors (TLRs) play a crucial role in the activation of innate immunity in response to many viruses. We previously reported the implication of TLR2 in the recognition of Epstein-Barr virus (EBV) by human monocytes. Because murine gammaherpesvirus-68 (MHV-68) is a useful model to study human gammaherpesvirus pathogenesis in vivo, we evaluated the importance of mouse TLR2 in the recognition of MHV-68.Methodology/Principal FindingsIn studies using transfected HEK293 cells, MHV-68 lead to the activation of NF-κB reporter through TLR2. In addition, production of interleukin-6 (IL-6) and interferon-α (IFN-α) upon MHV-68 stimulation was reduced in murine embryonic fibroblasts (MEFs) derived from TLR2−/− and MyD88−/− mice as compared to their wild type (WT) counterpart. In transgenic mice expressing a luciferase reporter gene under the control of the mTLR2 promoter, MHV-68 challenge activated TLR2 transcription. Increased expression levels of TLR2 on blood granulocytes (CD115−Gr1+) and inflammatory monocytes (CD115+Gr1+), which mobilized to the lungs upon infection with MHV-68, was also confirmed by flow cytometry. Finally, TLR2 or MyD88 deficiency was associated with decreased IL-6 and type 1 IFN production as well as increased viral burden during short-term challenges with MHV-68.Conclusions/SignificanceTLR2 contributes to the production of inflammatory cytokines and type 1 IFN as well as to the control of viral burden during infection with MHV-68. Taken together, our results suggest that the TLR2 pathway has a relevant role in the recognition of this virus and in the subsequent activation of the innate immune response.

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Section: Methodsmentioning

confidence: 99%

Involvement of TLR2 in Recognition of Acute Gammaherpesvirus-68 Infection

et al. 2010

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“…Various investigations have focused on a correlation between Epstein-Barr virus infection and cytokine expression. Although Epstein-Barr virus preferentially infects B cells, it is well known that the virus is capable of replicating in epithelial cells of the oro- Total A1 A2 A3 B1 B2 B3 C1 C2 C3 Controls 6 11 3 2 0 22 Not applicable HIV/no oral lesions 1 8 17 12 1 39 3 8 1 0 4 11 0 0 12 HIV/candidiasis 0 1 4 3 0 8 0 0 0 0 2 1 0 1 4 HIV/oral hairy leukoplakia 1 0 0 4 0 5 2 1 0 0 0 0 0 0 2 Total 8 20 24 21 1 5 9 1 0 6 12 0 1 18 pharynx, as well as binding monocytes and neutrophils (5,18,19). Thus, it is of no surprise that Epstein-Barr virus has been shown to support the expression of IL-1 and IL-1 receptor antagonist (2,41), IL-4 (38), IL-10 (6, 52), IL-8, tumor necrosis factor (TNF)-a and TNF-b (28).…”

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confidence: 99%

Cytokine profiles in parotid saliva from HIV‐1‐infected individuals: changes associated with opportunistic infections in the oral cavity

Black¹,

Merrill²,

Jackson³

et al. 2000

Oral Microbiology and Immunology

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The purpose of this study was to quantitate levels of cytokines in parotid saliva of subjects infected with human immunodeficiency virus-1 (HIV-1) and to determine if the cytokine profiles differ in subjects with an oral opportunistic infection, i.e., candidiasis or oral hairy leukoplakia. Parotid saliva samples were obtained from HIV-infected individuals with or without candidiasis or oral hairy leukoplakia and from healthy controls and were assessed by ELISA for levels of interleukin (IL)-1, IL-2, IL-4, IL-5, IL-10, transforming growth factor-beta, tumor necrosis factor-alpha and interferon (IFN)-gamma. Saliva from HIV-infected subjects with oral candidiasis had significantly higher levels of IFN-gamma than that seen in HIV-infected individuals with no oral disease and significantly higher levels of IL-2, IL-5 and IFN-gamma than saliva of healthy controls. No significant difference was seen in cytokine levels in saliva from HIV-infected subjects with no oral infections and healthy controls. The HIV-infected subjects with oral hairy leukoplakia displayed significantly higher levels of both IL-1 alpha and IFN-gamma compared with the HIV and no oral disease group and a higher level of IFN-gamma than seen in saliva from the healthy control group. In comparing cytokine levels from both HIV and oral disease groups, significant differences were detected in levels of IL-5 and IL-10. These results indicate that the profile of salivary cytokines is altered as a result of the oral opportunistic infection candidiasis or oral hairy leukoplakia and also by concurrent HIV infection.

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“…The cellular receptor involved in the interaction of the glycoprotein gp350 with the PMN surface has yet to be characterized. Previous data from our laboratory suggested that this receptor is distinct from the well-defined CD21 (CR2) antigen used by EBV for entry into B cells; indeed, the CD21 antigen is not expressed at the surface of PMN [9] and moreover anti-CD21 antibodies did not interfere with the attachment of EBV to PMN and monocytes [8,9]. At the present time, it is unknown if EBV uses the same alternative receptor on PMN and monocytes.…”

Section: Discussionmentioning

confidence: 84%

“…Increased LTB 4 biosynthesis could be a way for the virus to attract more PMN (and other leucocytes responsive to the chemotactic effect of LTB 4 ) at the site of infection. Previous results from our laboratory have shown that EBV induces expression of various chemokines and immunoregulatory molecules in monocytes and PMN [8,9,11,13] and it was suggested that up-regulation of MIP-1a , which is chemotactic for B cells, may enhance recruitment of B cells to the site of infection [13]. Thus, modulation of cytokines and leukotrienes in monocytes and PMN might be part of an important immune process which dictates the outcome of EBV infections.…”

Section: Discussionmentioning

confidence: 95%

Epstein–Barr virus primes human polymorphonuclear leucocytes for the biosynthesis of leukotriene B4

Gosselin¹,

Savard²,

Tardif³

et al. 2001

Clinical and Experimental Immunology

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SUMMARYIn the present study, we have investigated the effect of the short-term incubation of polymorphonuclear leucocytes (PMN) with infectious Epstein±Barr virus (EBV) on leukotriene B 4 (LTB 4 ) biosynthesis. Pre-exposure of PMN to EBV led to an increased production of LTB 4 upon stimulation with either the ionophore A23187, the chemotactic peptide fMLP, or phagocytic particles (zymosan). Experiments performed with viral particles pretreated with a neutralizing antibody raised against the gp350 of the viral envelope revealed that a specific interaction between the PMN surface and the viral glycoprotein gp350 is required for the priming effect of EBV. Preincubation of PMN with EBV resulted in an increased release of arachidonic acid upon stimulation with a second agonist. Moreover, LTB 4 biosynthesis in EBV/A23187-treated PMN was greatly diminished in the presence of an inhibitor of the cytosolic phospholipase A 2 (cPLA 2 ), suggesting that cPLA 2 plays a critical role in the priming effect of EBV. Accordingly, EBV by itself promoted Ser-505 phosphorylation of cPLA2 and strongly enhanced fMLP-induced phosphorylation of p38 MAP kinase, an enzyme known to phosphorylate cPLA 2 in human PMN. Furthermore, fMLP-induced translocation of cPLA 2 was strongly enhanced when PMN were previously exposed to EBV. These data indicate that binding of EBV to human PMN results in the activation of intracellular events involved in the release of pro-inflammatory lipid mediators.

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Epstein-Barr virus modulates de novo protein synthesis in human neutrophils

Cited by 16 publications

References 34 publications

Involvement of TLR2 in Recognition of Acute Gammaherpesvirus-68 Infection

Involvement of TLR2 in Recognition of Acute Gammaherpesvirus-68 Infection

Cytokine profiles in parotid saliva from HIV‐1‐infected individuals: changes associated with opportunistic infections in the oral cavity

Epstein–Barr virus primes human polymorphonuclear leucocytes for the biosynthesis of leukotriene B4

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