Classical swine fever virus induces tumor necrosis factor-a and lymphocyte apoptosis

2004 ◽  
Vol 149 (5) ◽  
pp. 875-889 ◽  
Author(s):  
C. Choi ◽  
K.-K. Hwang ◽  
C. Chae
Keyword(s):  
Tumor Necrosis Factor ◽  
Classical Swine Fever Virus ◽  
Tumor Necrosis ◽  
Classical Swine Fever ◽  
Fever Virus ◽  
Lymphocyte Apoptosis ◽  
Necrosis Factor

scholarly journals Cytokines regulate HIV-1 replication and lymphocyte apoptosis in vitro

2013 ◽  
Vol 94 (6) ◽  
pp. 906-910 ◽  
Author(s):  
S V Boichuk ◽  
P D Dunaev ◽  
I G Mustafin
Keyword(s):  
Flow Cytometry ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Lymphocyte Apoptosis ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Hiv 1 ◽  
Necrosis Factor

Aim. To study the ability of cytokines - interleukin-2, interleukin-7 and tumor necrosis factor alpha to induce human immunodeficiency virus type 1 (HIV-1) replication and lymphocyte apoptosis in vitro. Methods. Peripheral blood mononuclears were separated by centrifugation on a ficoll paque solution specific density gradient. Lymphocytes were cultivated in RPMI 1640 medium with addition of L-glutamine, embryonal bovine serum, antibiotics and cytokines (interleukines-2, -4, -7, tumor necrosis factor alpha). To infect the lymphocytes, a laboratory strain of HIV-1 NL4-3 (NIH ResReag. Prog., USA) was used. HIV-1 replication was assessed by р24gag viral protein level in culture supernatants (ELISA) and its cytozolic level in lymphocytes (flow cytometry). Lymphocyte apoptosis was assessed by flow cytometry using the following parameters: (1) decrease of transmembrane mitochondrial potential; (2) increase in phosphatidyl serine molecules expression. Lymphocyte activation was assessed by CD25 and HLA-DR molecules expression (flow cytometry). Results. Cytokines induce the HIV-1 replication in lymphocytes in vitro. HIV-1 replication was noted only if inactivated lymphocytes were present in the culture. At the same time, lymphocytes not expressing the classical activation markers (CD25 and HLA-DR) were present among the lymphocytes producing HIV-1 indicating the possible alternative mechanism of HIV-1 replication, not dependent on cell activation. This fact might also be an evidence of viral replication processes in the pool of latently-infected lymphocytes, not expressing the classic activation markers. The abovementioned cytokines promote apoptotic death of uninfected lymphocytes in vitro, backing up the infected cells viability and thus promoting HIV-1 replication. Conclusion. Cytokines (interleukines-2, -4, -7, tumor necrosis factor alpha) which are known as factors supporting the immune system homeostasis and immune response formation, might also play a negative role in HIV-1 pathogenesis - induce HIV-1 replication in lymphocytes and, probably, lead to reactivation of the pool of latently-infected lymphocytes, deepening the lymphopenia and leading to disease progression.

DECREASED LYMPHOCYTE APOPTOSIS BY ANTI-TUMOR NECROSIS FACTOR ANTIBODY IN PEYERʼS PATCHES AFTER SEVERE BURN

Shock ◽  
2003 ◽  
Vol 20 (1) ◽  
pp. 70-73 ◽  
Author(s):  
Kenneth J. Woodside ◽  
Marcus Spies ◽  
Xiao-wu Wu ◽  
Juquan Song ◽  
Shahnaz S. Quadeer ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Lymphocyte Apoptosis ◽  
Severe Burn ◽  
Necrosis Factor

scholarly journals TNF-Mediated Inhibition of Classical Swine Fever Virus Replication Is IRF1-, NF-κB- and JAK/STAT Signaling-Dependent

Viruses ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 2017
Author(s):  
Matthias Liniger ◽  
Markus Gerber ◽  
Sandra Renzullo ◽  
Obdulio García-Nicolás ◽  
Nicolas Ruggli
Keyword(s):  
Signaling Pathways ◽  
Classical Swine Fever Virus ◽  
Proinflammatory Cytokine ◽  
Classical Swine Fever ◽  
Antiviral Effect ◽  
Fever Virus ◽  
Type I ◽  
Type I Ifn ◽  
Interferon Regulatory Factor 1 ◽  
Necrosis Factor

The sera from pigs infected with virulent classical swine fever virus (CSFV) contain substantial amounts of tumor necrosis factor (TNF), a prototype proinflammatory cytokine with pleiotropic activities. TNF limits the replication of CSFV in cell culture. In order to investigate the signaling involved in the antiviral activity of TNF, we employed small-molecule inhibitors to interfere specifically with JAK/STAT and NF-κB signaling pathways in near-to-primary endothelial PEDSV.15 cells. In addition, we knocked out selected factors of the interferon (IFN) induction and signaling pathways using CRISPR/Cas9. We found that the anti-CSFV effect of TNF was sensitive to JAK/STAT inhibitors, suggesting that TNF induces IFN signaling. Accordingly, we observed that the antiviral effect of TNF was dependent on intact type I IFN signaling as PEDSV.15 cells with the disrupted type I IFN receptor lost their capacity to limit the replication of CSFV after TNF treatment. Consequently, we examined whether TNF activates the type I IFN induction pathway. With genetically modified PEDSV.15 cells deficient in functional interferon regulatory factor 1 or 3 (IRF1 or IRF3), we observed that the anti-CSFV activity exhibited by TNF was dependent on IRF1, whereas IRF3 was dispensable. This was distinct from the lipopolysaccharide (LPS)-driven antiviral effect that relied on both IRF1 and IRF3. In agreement with the requirement of IRF1 to induce TNF- and LPS-mediated antiviral effects, intact IRF1 was also essential for TNF- and LPS-mediated induction of IFN-β mRNA, while the activation of NF-κB was not dependent on IRF1. Nevertheless, NF-κB activation was essential for the TNF-mediated antiviral effect. Finally, we observed that CSFV failed to counteract the TNF-mediated induction of the IFN-β mRNA in PEDSV.15 cells, suggesting that CSFV does not interfere with IRF1-dependent signaling. In summary, we report that the proinflammatory cytokine TNF limits the replication of CSFV in PEDSV.15 cells by specific induction of an IRF1-dependent antiviral type I IFN response.

scholarly journals Mechanisms of lymphocyte apoptosis at tick-borne encephalitis

2011 ◽  
Vol 10 (6) ◽  
pp. 61-65
Author(s):  
O. Ye. Chechina ◽  
N. V. Ryazantseva ◽  
Ye. V. Sazonova ◽  
N. G. Zhukova ◽  
I. N. Udintseva ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Transmembrane Potential ◽  
Mitochondrial Transmembrane Potential ◽  
Lymphocyte Apoptosis ◽  
Factor I ◽  
Tick Borne Encephalitis ◽  
Necrosis Factor

Results of the complex research of apoptosis realization of lymphocytes at acute tick-born encephalitis and during long antigenemia condition has been presented in this article. The acceleration of apoptosis, tumor necrosis factor I presentation and the decrease in mitochondrial transmembrane potential of lymphocytes were determined at tick-born encephalitis. Uncovered changes are more appeared at acute neuroinfection.

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