Tumor Necrosis Factor Alpha Exerts Powerful Anti-Influenza Virus Effects in Lung Epithelial Cells

doi:10.1128/JVI.76.3.1071-1076.2002

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Tumor Necrosis Factor Alpha Exerts Powerful Anti-Influenza Virus Effects in Lung Epithelial Cells

Journal Article•DOI•

Tumor Necrosis Factor Alpha Exerts Powerful Anti-Influenza Virus Effects in Lung Epithelial Cells

Sang Heui Seo¹, Robert G. Webster¹•Institutions (1)

St. Jude Children's Research Hospital¹

01 Feb 2002-Journal of Virology (American Society for Microbiology)-Vol. 76, Iss: 3, pp 1071-1076

TL;DR: TNF-α showed strong antiviral activity against avian, swine, and human influenza viruses, and the antiviral effect of TNF- α was greater than that of gamma or alpha interferon.

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Abstract: Previous studies have associated influenza virus-induced expression of inflammatory cytokines, including tumor necrosis factor alpha (TNF-α), with influenza pathogenesis in the human respiratory tract and have suggested that alpha and beta interferons are the first cytokines recruited to counteract such infection. However, we report here that TNF-α has powerful anti-influenza virus activity. When infected with influenza virus, cultured porcine lung epithelial cells expressed TNF-α in a dose-dependent manner. Expression of TNF-α was induced only by replicating virus. TNF-α showed strong antiviral activity against avian, swine, and human influenza viruses, and the antiviral effect of TNF-α was greater than that of gamma or alpha interferon. These findings suggest that TNF-α serves as the first line of defense against influenza virus infection in the natural host.

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Journal Article•DOI•

Into the Eye of the Cytokine Storm

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Jennifer R. Tisoncik¹, Marcus J. Korth¹, Cameron P. Simmons², Jeremy Farrar², Thomas R. Martin¹, Michael G. Katze¹ - Show less +2 more•Institutions (2)

University of Washington¹, University of Oxford²

01 Mar 2012-Microbiology and Molecular Biology Reviews

TL;DR: How high-throughput genomic methods are revealing the importance of the kinetics of cytokine gene expression and the remarkable degree of redundancy and overlap in cytokine signaling is highlighted.

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Abstract: The cytokine storm has captured the attention of the public and the scientific community alike, and while the general notion of an excessive or uncontrolled release of proinflammatory cytokines is well known, the concept of a cytokine storm and the biological consequences of cytokine overproduction are not clearly defined. Cytokine storms are associated with a wide variety of infectious and noninfectious diseases. The term was popularized largely in the context of avian H5N1 influenza virus infection, bringing the term into popular media. In this review, we focus on the cytokine storm in the context of virus infection, and we highlight how high-throughput genomic methods are revealing the importance of the kinetics of cytokine gene expression and the remarkable degree of redundancy and overlap in cytokine signaling. We also address evidence for and against the role of the cytokine storm in the pathology of clinical and infectious disease and discuss why it has been so difficult to use knowledge of the cytokine storm and immunomodulatory therapies to improve the clinical outcomes for patients with severe acute infections.

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1,501 citations

Cites background or result from "Tumor Necrosis Factor Alpha Exerts ..."

...The concept of secondary effects of cytokine cascades, as opposed to the direct effect of the virus, in amplifying and broadening the proinflammatory response may be important in the escalation of cytokine storm (24, 111, 125)....
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...It is highly expressed across infection models, including primary human respiratory epithelial cells (24, 125) and human monocyte-derived macrophages (26, 59, 62), compared with during seasonal H1N1 influenza virus and swine-origin H1N1 influenza virus (SOIV) infection (111)....
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Journal Article•DOI•

Lethal H5N1 influenza viruses escape host anti-viral cytokine responses.

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Sang Heui Seo¹, Erich Hoffmann¹, Robert G. Webster¹•Institutions (1)

St. Jude Children's Research Hospital¹

26 Aug 2002-Nature Medicine

TL;DR: It is shown that lethal H5N1 influenza virus, unlike other human, avian and swine influenza viruses, are resistant to the antiviral effects of interferons and tumor necrosis factor α, and the nonstructural (NS) gene of H5n1 viruses is associated with this resistance.

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Abstract: The H5N1 influenza viruses transmitted to humans in 1997 were highly virulent, but the mechanism of their virulence in humans is largely unknown. Here we show that lethal H5N1 influenza viruses, unlike other human, avian and swine influenza viruses, are resistant to the antiviral effects of interferons and tumor necrosis factor alpha. The nonstructural (NS) gene of H5N1 viruses is associated with this resistance. Pigs infected with recombinant human H1N1 influenza virus that carried the H5N1 NS gene experienced significantly greater and more prolonged viremia, fever and weight loss than did pigs infected with wild-type human H1N1 influenza virus. These effects required the presence of glutamic acid at position 92 of the NS1 molecule. These findings may explain the mechanism of the high virulence of H5N1 influenza viruses in humans.

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659 citations

Cites background from "Tumor Necrosis Factor Alpha Exerts ..."

...Although both innate and induced immune responses are thought to have a role in virus clearance, IFNs and TNF-α are the first line of defense against the replication of influenza viruse...
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Journal Article•DOI•

Glycan Microarray Analysis of the Hemagglutinins from Modern and Pandemic Influenza Viruses Reveals Different Receptor Specificities

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James Stevens¹, Ola Blixt¹, Laurel Glaser², Jeffery K. Taubenberger³, Peter Palese², James C. Paulson¹, Ian A. Wilson¹ - Show less +3 more•Institutions (3)

Scripps Research Institute¹, Icahn School of Medicine at Mount Sinai², Armed Forces Institute of Pathology³

03 Feb 2006-Journal of Molecular Biology

TL;DR: The species barrier, as defined by the receptor specificity preferences of 1918 human viruses compared to likely avian virus progenitors, can be circumvented by changes at only two positions in the HA receptor binding site.

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645 citations

Journal Article•DOI•

Interferons α and λ Inhibit Hepatitis C Virus Replication With Distinct Signal Transduction and Gene Regulation Kinetics

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Tobias Marcello¹, Arash Grakoui², Giovanna Barba-Spaeth¹, Erica S. Machlin¹, Sergei V. Kotenko³, Margaret R. MacDonald¹, Charles M. Rice¹ - Show less +3 more•Institutions (3)

Rockefeller University¹, Emory University², Rutgers University³

01 Dec 2006-Gastroenterology

TL;DR: Dose- and time-dependent HCV inhibition and kinetics of IFN-λ-mediated signal transducers and activators of transcription (STAT) activation and induction of potential effector genes were distinct from those ofIFN-α.

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557 citations

Journal Article•DOI•

MERS-CoV infection in humans is associated with a pro-inflammatory Th1 and Th17 cytokine profile.

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Waleed H. Mahallawi¹, Omar F. Khabour², Qibo Zhang³, Hatim M. Makhdoum¹, Bandar A. Suliman¹ - Show less +1 more•Institutions (3)

Taibah University¹, Jordan University of Science and Technology², University of Liverpool³

02 Feb 2018-Cytokine

TL;DR: A prominent pro‐inflammatory Th1 and Th17 response was clearly seen in patients with MERS‐CoV infection, with markedly increased concentrations of IFN‐&ggr;, TNF‐&agR;, IL‐15 and IL‐17 compared to controls.

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490 citations

Cites background from "Tumor Necrosis Factor Alpha Exerts ..."

...Previous studies showed that TNF-α exerts a strong antiviral activity against avian, swine, and human influenza viruses [50]....
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References

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Open Access

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Journal Article•DOI•

An endotoxin-induced serum factor that causes necrosis of tumors

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Elizabeth A. Carswell, Lloyd J. Old, R. L. Kassel, Saul Green, N Fiore, Barbara Williamson - Show less +2 more

01 Sep 1975-Proceedings of the National Academy of Sciences of the United States of America

TL;DR: It is proposed that TNF mediates endotoxin-induced tumor necrosis, and that it may be responsible for the suppression of transformed cells by activated macrophages.

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Abstract: In studying "hemorrhagic necrosis" of tumors produced by endotoxin, it was found that the serum of bacillus Calmette--Guerin (BCG)-infected mice treated with endotoxin contains a substance (tumor necrosis factor; TNF) which mimics the tumor necrotic action of endotoxin itself. TNF-positive serum is as effective as endotoxin itself in causing necrosis of the sarcoma Meth A and other transplanted tumors. A variety of tests indicate that TNF is not residual endotoxin, but a factor released from host cells, probably macrophages, by endotoxin. Corynebacteria and Zymosan, which like BCG induce hyperplasia of the reticulo-endothelial system, can substitute for BCG in priming mice for release of TNF by endotoxin. TNF is toxic in vitro for two neoplastic cell lines; it is not toxic for mouse embryo cultures. We propose that TNF mediates endotoxin-induced tumor necrosis, and that it may be responsible for the suppression of transformed cells by activated macrophages.

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4,490 citations

"Tumor Necrosis Factor Alpha Exerts ..." refers background in this paper

...Although TNF- was first noted for its role in the killing of tumor cells (5), it has pleiotropic functions that include the inflammatory response and host resistance to pathogens (1)....
[...]

Book•

Cellular and Molecular Immunology

[...]

Abul K. Abbas, Andrew H. Lichtman, Shiv Pillai

01 Jan 1994

TL;DR: Cellular and molecular immunology , Cellular and molecular Immunology , کتابخانه الکرونیک و دیجیتال - آذرسا

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Abstract: Cellular and molecular immunology , Cellular and molecular immunology , کتابخانه الکترونیک و دیجیتال - آذرسا

...read moreread less

3,968 citations

Journal Article•DOI•

Cellular and Molecular Immunology

[...]

A.M. Denman

01 Apr 1992-Postgraduate Medical Journal

TL;DR: This sales letter may not influence you to be smarter, but the book that the authors offer will evoke you to being smarter and you'll know more than others who don't.

...read moreread less

Abstract: This sales letter may not influence you to be smarter, but the book that we offer will evoke you to be smarter. Yeah, at least you'll know more than others who don't. This is what called as the quality life improvisation. Why should this cellular and molecular immunology? It's because this is your favourite theme to read. If you like this theme about, why don't you read the book to enrich your discussion?

...read moreread less

1,562 citations

"Tumor Necrosis Factor Alpha Exerts ..." refers background in this paper

...TNF- is produced by activated macrophages, T and B lymphocytes, natural killer cells, astrocytes, endothelial cells, smooth muscle cells, some tumor cells, and epithelial cells (1, 2)....
[...]
...Macrophages, unlike epithelial cells, can engulf and degrade foreign antigens, leading to cytokine induction (1)....
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...This powerful inflammatory cytokine’s role in recruiting various host cells, including monocytes and T and B lymphocytes, to sites of infection (1) suggests that TNF- plays an important role in clearing influenza virus infection in the respiratory tract before the secondary immune response is activated....
[...]
...produce a considerable amount of TNF- in an infected host (1)....
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...Although TNF- was first noted for its role in the killing of tumor cells (5), it has pleiotropic functions that include the inflammatory response and host resistance to pathogens (1)....
[...]

Journal Article•DOI•

Tumor necrosis factor alpha and interleukin 1 stimulate the human immunodeficiency virus enhancer by activation of the nuclear factor kappa B

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Laurelee Osborn¹, Steven L. Kunkel¹, Gary J. Nabel¹•Institutions (1)

University of Michigan¹

01 Apr 1989-Proceedings of the National Academy of Sciences of the United States of America

TL;DR: It is demonstrated that two different peptide hormones, or cytokines, stimulate the human immunodeficiency virus enhancer, and this effect is mediated by nuclear factor (NF) kappa B (nuclear factor that binds the kappa immunoglobulin light chain gene enhancer); this link between binding at the surface membrane and stimulation of a specific transcription factor should help define intermediates for these cytokine activation pathways.

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Abstract: Binding of peptide hormones to surface membrane receptors leads to the transcription of specific genes within relevant target cells. How these signals are transduced to alter gene expression is largely unknown, but this mechanism probably involves a sequence of enzymatic steps that activate factors in the nucleus that modulate transcription. We now demonstrate that two different peptide hormones, or cytokines, stimulate the human immunodeficiency virus enhancer, and this effect is mediated by nuclear factor (NF) kappa B (nuclear factor that binds the kappa immunoglobulin light chain gene enhancer). These cytokines, tumor necrosis factor alpha and interleukin 1, act on multiple cell types and represent the only naturally occurring activators of this transcription factor among eight cytokines examined. Although NF-kappa B binding can be stimulated by phorbol 12-myristate 13-acetate, tumor necrosis factor alpha acts through an independent mechanism, inducing NF-kappa B binding in HT-2 cells, which did not show increased binding in response to phorbol 12-myristate 13-acetate, and causing superinduction in Jurkat T-lymphoma cells. Tumor necrosis factor alpha is also a more selective activator of T cells than phorbol 12-myristate 13-acetate, having no effect on lymphokine production in EL-4 cells at the same time it induces NF-kappa B. These findings suggest that human immunodeficiency virus gene expression can be induced in T cells without activating lymphokine secretion and that the role of these cytokines in the activation of latent human immunodeficiency virus infection deserves further clinical evaluation. Finally, this link between binding at the surface membrane and stimulation of a specific transcription factor should help define intermediates for these cytokine activation pathways.

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1,559 citations

"Tumor Necrosis Factor Alpha Exerts ..." refers background in this paper

...However, although TNF- inhibited the replication of human immunodeficiency virus type 1 (HIV- 1) in peripheral blood monocytes and alveolar macrophages (18, 27), it could also stimulate HIV-1 replication in chronically infected T cells and promonocytic cell lines (7, 8, 33 )....
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Journal Article•DOI•

Influenza A Virus Lacking the NS1 Gene Replicates in Interferon-Deficient Systems

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Adolfo García-Sastre¹, Andrej Egorov, Demetrius Matassov¹, Sabine Brandt², David E. Levy³, Joan E. Durbin⁴, Peter Palese¹, Thomas Muster² - Show less +4 more•Institutions (4)

Icahn School of Medicine at Mount Sinai¹, University of Vienna², New York University³, Hospital Research Foundation⁴

20 Dec 1998-Virology

TL;DR: In this paper, a viable transfectant influenza A virus (delNS1) which lacks the NS1 gene has been generated through the use of reverse genetics, and it has been shown that the NS 1 protein plays a crucial role in inhibiting interferon-mediated antiviral responses of the host.

...read moreread less

998 citations