Effect of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) on Influenza Virus Host Resistance in Mice

Burleson, Gary R.; Lebrec, Hervé; Yang, Yung; Ibanes, Joelle D.; Pennington, Kevin N.; Birnbaum, Linda S.

doi:10.1006/faat.1996.0004

Cited by 112 publications

(26 citation statements)

References 39 publications

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“…For example, with influenza A virus infection AhR activation by the administration of TCDD decreased the survival time to lethal infection and resulted in mortality with a non lethal dose of the virus [42], [43]. The cause of lethality was unclear since TCDD treated animals cleared the virus from the lungs as well as a non treated mice [44]. More than likely animals succumbed to lung pathology associated with increased neutrophilia found in the lungs of TCDD treated mice [21], [45].…”

Section: Discussionmentioning

confidence: 99%

Controlling Viral Immuno-Inflammatory Lesions by Modulating Aryl Hydrocarbon Receptor Signaling

Veiga-Parga

Suryawanshi²,

Rouse

2011

PLoS Pathog

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Ocular herpes simplex virus infection can cause a blinding CD4+ T cell orchestrated immuno-inflammatory lesion in the cornea called Stromal Keratitis (SK). A key to controlling the severity of SK lesions is to suppress the activity of T cells that orchestrate lesions and enhance the representation of regulatory cells that inhibit effector cell function. In this report we show that a single administration of TCDD (2, 3, 7, 8- Tetrachlorodibenzo-p-dioxin), a non-physiological ligand for the AhR receptor, was an effective means of reducing the severity of SK lesions. It acted by causing apoptosis of Foxp3- CD4+ T cells but had no effect on Foxp3+ CD4+ Tregs. TCDD also decreased the proliferation of Foxp3- CD4+ T cells. The consequence was an increase in the ratio of Tregs to T effectors which likely accounted for the reduced inflammatory responses. In addition, in vitro studies revealed that TCDD addition to anti-CD3/CD28 stimulated naïve CD4+ T cells caused a significant induction of Tregs, but inhibited the differentiation of Th1 and Th17 cells. Since a single TCDD administration given after the disease process had been initiated generated long lasting anti-inflammatory effects, the approach holds promise as a therapeutic means of controlling virus induced inflammatory lesions.

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Section: Discussionmentioning

confidence: 99%

Controlling Viral Immuno-Inflammatory Lesions by Modulating Aryl Hydrocarbon Receptor Signaling

Veiga-Parga

Suryawanshi²,

Rouse

2011

PLoS Pathog

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“…Although cellular and molecular mechanisms of TCDD immunotoxicity are not well understood, suppressed humoral and cell-mediated immune responses and decreased host resistance to infectious disease have been observed in experimental animals [1,2]. In particular, several studies indicated that TCDD exposure leads to an enhanced mortality in mice infected with influenza virus [3], increased gene expression of human immunodeficiency virus type-1 (HIV-1) in chronically infected cells [4], and an activation of cytomegalovirus replication in human fibroblasts [5]. Furthermore, TCDD activates HIV-1 replication in OM 10.1 cells, promyelocytic cell line latently infected with HIV-1 [6], and enhances Bovine Herpesvirus type-1 (BHV-1) replication in bovine cells [7].…”

Section: Introductionmentioning

confidence: 97%

2,3,7,8-Tetrachlorodibenzo-p-dioxin regulates Bovine Herpesvirus type 1 induced apoptosis by modulating Bcl-2 family members

et al. 2008

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Exposure to environmental contaminants, like 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), leads to an increased susceptibility to infectious agents. Infection of bovine cells (MDBK) with Bovine Herpesvirus 1 (BHV-1) anticipates virus-induced apoptosis, suggesting an involvement of TCDD in virus infection. Herein we analyzed the effects of TCDD on apoptotic pathway in MDBK cells infected with BHV-1. After 12 h of infection, TCDD induced a significant increase in apoptotic cells. TCDD caused a dose-dependent up-regulation and anticipated activation of caspases 3, 8 and 9, with respect to unexposed groups. TCDD anticipated cleavage of PARP, compared to controls. Furthermore TCDD increased Bax and Bid levels, and decreased Bcl-2 and Bcl-XL levels. Such events took place earlier in exposed than unexposed cells. These results showed that TCDD influences BHV-1 induced apoptosis through members of Bcl-2 family and up-regulating activation of caspases.

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“…TCDD causes a broad range of immunologic effects in experimental animals, including decreased host resistance to infectious disease and suppressed humoral and cell-mediated immune responses [4]. In particular, it has been demonstrated that TCDD exposure leads to an enhanced mortality in mice infected with influenza virus [5], increased gene expression of human immunodeficiency virus type-1 (HIV-1) in chronically infected cells [6], and an activation of cytomegalovirus replication in human fibroblasts [7]. Moreover, TCDD activates HIV-1 replication in a promyelocytic cell line latently infected with HIV-1 [8], and enhances BHV-1 replication in a bovine cell line [9].…”

Section: Introductionmentioning

confidence: 99%

2,3,7,8-Tetrachlorodibenzo-p-Dioxin Promotes BHV-1 Infection in Mammalian Cells by Interfering with Iron Homeostasis Regulation

et al. 2013

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Mammalian cells require iron to satisfy metabolic needs or to accomplish specialized functions, and DNA viruses, like bovine herpesvirus 1 (BHV-1), require an iron-replete host to efficiently replicate, so that iron bioavailability is an important component of viral virulence. Cellular iron metabolism is coordinately controlled by the Iron Regulatory Proteins (IRP1 and IRP2), whose activity is affected by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a current and persistent environmental contaminant. Considering that TCDD enhances BHV-1 replication, herein we analyzed the effects of TCDD on iron metabolism during BHV-1 infection in MDBK cells, and presented evidences of a divergent modulation of IRP1 and IRP2 RNA-binding capacity. Moreover, an up-regulation of transferrin receptor 1 (TfR1) and a concomitant down-regulation of ferritin were observed. This scenario led to an expansion of the labile iron pool (LIP) and induces a significant enhance of viral titer, as confirmed by increased levels of BHV-1 infected cell protein 0 (bICP0), the major transcriptional regulatory protein of BHV-1. Taken together, our data suggest that TCDD increases the free intracellular iron availability thereby promoting the onset of BHV-1 infection and rendering bovine cells more vulnerable to the virus.

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Effect of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) on Influenza Virus Host Resistance in Mice

Cited by 112 publications

References 39 publications

Controlling Viral Immuno-Inflammatory Lesions by Modulating Aryl Hydrocarbon Receptor Signaling

Controlling Viral Immuno-Inflammatory Lesions by Modulating Aryl Hydrocarbon Receptor Signaling

2,3,7,8-Tetrachlorodibenzo-p-dioxin regulates Bovine Herpesvirus type 1 induced apoptosis by modulating Bcl-2 family members

2,3,7,8-Tetrachlorodibenzo-p-Dioxin Promotes BHV-1 Infection in Mammalian Cells by Interfering with Iron Homeostasis Regulation

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