Inhibition of Sindbis virus replication by cyclopentenone prostaglandins: A cell-mediated event associated with heat-shock protein synthesis

Mastromarino, Paola; Conti, Cinzia; Petruzziello, R.; Marco, Alessandra De; Pica, Francesca; Santoro, M.

doi:10.1016/0166-3542(93)90021-a

Cited by 34 publications

(26 citation statements)

References 23 publications

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“…For example, the J series PGs can inhibit viral replication and prevent the establishment of persistent viral infections (53). Antiviral effects have been shown against both DNA and RNA viruses, including herpesviruses (54), togaviruses (55), and rhabdoviruses (56). More recent work has focused on the effects of cyclopentenone PGs on the HIV virus.…”

Section: Discussionmentioning

confidence: 99%

15-Deoxy-Δ12,1412,14-PGJ2 Induces IL-8 Production in Human T Cells by a Mitogen-Activated Protein Kinase Pathway

Harris

Smith

Phipps

2002

The Journal of Immunology

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Mast cells, platelets, and some macrophages are abundant sources of PGD2 and its active metabolite 15-deoxy-Δ12,14-PGJ2 (15-d-PGJ2). The lipid mediator 15-d-PGJ2 regulates numerous processes, including adipogenesis, apoptosis, and inflammation. The 15-d-PGJ2 has been shown to both inhibit as well as induce the production of inflammatory mediators such as TNF-α, IL-1β, and cyclooxygenase, mostly occurring via a nuclear receptor called peroxisome proliferator-activated receptor-γ (PPAR-γ). Data concerning the effects of 15-d-PGJ2 on human T cells and immune regulation are sparse. IL-8, a cytokine with both chemotactic and angiogenic effects, is produced by T lymphocytes following activation. Whether 15-d-PGJ2 can regulate the production of IL-8 in T cells in unknown. Interestingly, 15-d-PGJ2 treatment of unstimulated T cells induces cell death. In contrast, in activated human T lymphocytes, 15-d-PGJ2 does not kill them, but induces the synthesis of IL-8. In this study, we report that 15-d-PGJ2 induced a significant increase in both IL-8 mRNA and protein from activated human T lymphocytes. The induction of IL-8 by 15-d-PGJ2 did not occur through the nuclear receptor PPAR-γ, as synthetic PPAR-γ agonists did not mimic the IL-8-inducing effects of 15-d-PGJ2. The mechanism of IL-8 induction was through a mitogen-activated protein kinase and NF-κB pathway, as inhibitors of both systems abrogated IL-8 protein induction. Therefore, 15-d-PGJ2 can act as a potent proinflammatory mediator in activated T cells by inducing the production of IL-8. These findings show the complexity with which 15-d-PGJ2 regulates T cells by possessing both pro- and anti-inflammatory properties depending on the activation state of the cell. The implications of this research also include that caution is warranted in assigning a solely anti-inflammatory role for 15-d-PGJ2.

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Section: Discussionmentioning

confidence: 99%

15-Deoxy-Δ12,1412,14-PGJ2 Induces IL-8 Production in Human T Cells by a Mitogen-Activated Protein Kinase Pathway

Harris

Smith

Phipps

2002

The Journal of Immunology

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“…Data from the literature are still insufficient to identify a mechanism of action of Pgs as antiviral agents, although recent investigations have shown that the antiviral activity of Pgs is associated with the induction of 70-kDa heat shock proteins synthesis (19). We have previously observed that PGA 1 not only inhibits the replication of Mayaro virus in A. albopictus cells, but also stimulates the synthesis of several cellular polypeptides with molecular weights of 70, 57 and 23 kDa (20).…”

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confidence: 99%

Inhibition of Mayaro virus replication by prostaglandin A1 and B2 in Vero cells

Ishimaru

Marcicano

Rebello

1998

Braz J Med Biol Res

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The effect of prostaglandins (PGA 1 and PGB 2 ) on the replication of Mayaro virus was studied in Vero cells. PGA 1 and PGB 2 antiviral activity was found to be dose-dependent. However, while 10 µg/ml PGB 2 inhibited virus yield by 60%, at the same dose PGA 1 suppressed virus replication by more than 90%. SDS-PAGE analysis of [ 35 S]-methionine-labelled proteins showed that PGA 1 did not alter cellular protein synthesis. In infected cells, PGA 1 slightly inhibited the synthesis of protein C, while drastically inhibiting the synthesis of glycoproteins E 1 and E 2 .

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“…Several RNA viruses, including the paramyxovirus Sendai [13], the rhabdovirus vesicular stomatitis virus [14], and the togavirus Sindbis [34], have previously been shown not to affect PGA 1 -induced HSP70 synthesis in human or primate cells when treatment was started soon after infection. On the other hand, other RNA viruses, including poliovirus [21] and recently rotavirus [23], were found to prevent HSP70 synthesis induced by PGA 1.…”

Section: Discussionmentioning

confidence: 99%

Induction of the heat‐shock response by antiviral prostaglandins in human cells infected with human immunodeficiency virus type 1

Marco

Carattoli²,

Rozera³

et al. 1998

European Journal of Biochemistry

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Cyclopentenone prostaglandins inhibit the replication of several DNA and RNA viruses, including retroviruses. The antiviral activity has been associated with the induction of a 70-kDa heat-shock protein (HSP70), via activation of the heat-shock transcription factor (HSF) in infected cells. In the present study we investigated the effect of prostaglandin A 1 (PGA 1 ) on the regulation of HSP70 gene expression as well as on viral RNA and protein synthesis in CEM-SS cells during acute infection with human immunodeficiency virus type 1 (HIV-1). We report that HIV-1 infection does not alter HSF activation by PGA 1 , whereas it causes an increase in intracellular HSP70 mRNA levels, as a result of enhanced HSP70 mRNA stability. We also show that, as reported in studies of different virus/host cell models, PGA 1 inhibits HIV-1 replication by acting at multiple levels during HIV-1 infection. In addition to the previously reported block of HIV-1 mRNA transcription, PGA 1 was also found to inhibit viral protein synthesis. These results, together with the fact that prostaglandins are used clinically in the treatment of several diseases, open new perspectives in the search for novel antiretroviral drugs.Keywords : antiviral ; heat-shock factor ; heat-shock protein; human immunodeficiency virus; prostaglandin.Prostaglandins (PGs) function as intracellular signal mediators, participating in the regulation of a variety of physiological and pathological processes in eukaryotes, including inflammation and the febrile response [1], cell proliferation and differentiation [2], cytoprotection [3] and the immune response [4]. Starting from the observation that prostaglandins of the A type inhibit Sendai virus replication in cultured monkey cells [5], it is now well established that prostaglandins containing an A,β-unsaturated carbonyl group in the cyclopentane ring structure (cyclopentenone prostaglandins) possess potent antiviral activity against a wide variety of DNA and RNA viruses (reviewed in [6]). In the case of retroviruses, prostaglandins of the A and J types have been shown to inhibit the replication of human immunodeficiency virus-type 1 (HIV-1) in chronically infected human macrophages, and in a variety of acutely infected human cell lines [7Ϫ9].Even though in the last decade major advances have been made in the identification of the cellular and viral targets of cyclopentenone prostaglandins, the mechanism of their antiviral activity has not yet been completely elucidated. Cyclopentenone prostaglandins appear to function differently from any other known antiviral agent, acting at multiple levels during the virus Correspondence to

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Inhibition of Sindbis virus replication by cyclopentenone prostaglandins: A cell-mediated event associated with heat-shock protein synthesis

Cited by 34 publications

References 23 publications

15-Deoxy-Δ12,1412,14-PGJ2 Induces IL-8 Production in Human T Cells by a Mitogen-Activated Protein Kinase Pathway

15-Deoxy-Δ12,1412,14-PGJ2 Induces IL-8 Production in Human T Cells by a Mitogen-Activated Protein Kinase Pathway

Inhibition of Mayaro virus replication by prostaglandin A1 and B2 in Vero cells

Induction of the heat‐shock response by antiviral prostaglandins in human cells infected with human immunodeficiency virus type 1

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