TNF-α exerts potent anti-rotavirus effects via the activation of classical NF-κB pathway

Hakim, Mohamad S.; Ding, Shihao; Chen, Sunrui; Yin, Yuebang; Su, Junhong; Woude, C. Janneke van der; Fuhler, Gwenny M.; Peppelenbosch, Maikel P.; Pan, Qiuwei; Wang, Wenshi

doi:10.1016/j.virusres.2018.05.022

Cited by 34 publications

(31 citation statements)

References 47 publications

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“…In addition, Akt has also been linked to the regulation of Grx1 [45,46], which was also observed in the present study. TNFα is a downstream proinflammatory factor of NF-κB, which was confirmed to be necessary for liver injury induced by ethanol [47]. In the current study, Grx1 ablation further consolidated ethanolinduced increases in TNF-α mRNA and protein levels, which was normalized by blocking NF-κB, confirming the current hypothesis.…”

Section: Discussionsupporting

confidence: 86%

Contribution of glutaredoxin-1 to Fas s-glutathionylation in ethanol-induced liver injury

X¹,

Deng²,

Zhang³

et al. 2020

Preprint

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Background The reversible glutathionylation modification (PSSG) of Fas augments apoptosis, which can be reversed by the cytosolic deglutathionylation enzyme glutaredoxin-1 (Grx1), but its roles in alcoholic liver injury remain unknown. Therefore, the objective of this study was to investigate the impact of genetic ablation of Grx1 on Fas-SSG in regulating ethanol-induced injury. Methods The role of Grx1 in alcoholic liver injury was investigated in Grx1 knockout mice. Alcoholic liver injury was achieved by feeding mice with a liquid diet containing 5% ethanol for 2 weeks. Results We demonstrated that ethanol-fed mice had increased Grx1 activity and oxidative damage in the liver. On the other hand, Grx1-deficient mice had more serious liver damage when exposed to ethanol compared to that of wild-type mice, accompanied by increased alanine aminotransferase and aspartate aminotransferase levels, Fas-SSG, cleaved caspase-3 and hepatocyte apoptosis. Grx1 ablation resulted in the suppression of ethanol-induced nuclear factor-κB (NF-κB) signaling, its downstream signal, and Akt signaling cascades, which are required for protection against Fas-mediated apoptosis. Accordingly, blocking NK-κB prevented Fas-induced apoptosis in WT mice but not Grx1-/- mice. Furthermore, the number of Kupffer cells and related proinflammatory cytokines, including Akt, were lower in Grx1-/- livers than those of the controls. Conclusions Grx1 is essential for adaptation to alcohol exposure-induced oxidative injury by modulating Fas-SSG and Fas-induced apoptosis.

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Section: Discussionsupporting

confidence: 86%

Contribution of glutaredoxin-1 to Fas s-glutathionylation in ethanol-induced liver injury

X¹,

Deng²,

Zhang³

et al. 2020

Preprint

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“…Intestinal epithelial cells produce a variety of cytokines and chemokines in response to the viral attack, including IL-6, IL-8, TNF-α, and granulocyte-macrophage colony-stimulating factor. The production of those inflammatory factors is important for the protection against the viral infection through their direct antiviral effects (33) or the recruitment and activation of phagocytes (34). However, infiltration of immune cells to the intestinal mucosa can contribute to the local damage mediated by the inflammatory and oxidative stress (35).…”

Section: Discussionmentioning

confidence: 99%

Efficient Selection of New Immunobiotic Strains With Antiviral Effects in Local and Distal Mucosal Sites by Using Porcine Intestinal Epitheliocytes

et al. 2020

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“…Interestingly, our results suggest that infliximab treatment resulted in inhibition of TNFR/NF-κB signaling in an early life trauma-dependent manner, similar to the overall effects in this clinical trial. Results from preclinical and clinical studies have consistently documented that TNF antagonists modulate NF-κB activity in diverse tissues [31,[44][45][46][47][48]. TNF-α is a pro-inflammatory cytokine that exerts its effects by binding to two cell-surface receptors (TNFRs 1 and 2), which, through activation of downstream mediators, result in activation of NF-κB.…”

Section: Discussionmentioning

confidence: 99%

Extracellular Vesicle Biomarkers Reveal Inhibition of Neuroinflammation by Infliximab in Association with Antidepressant Response in Adults with Bipolar Depression

Mansur

Delgado-Peraza

Subramaniapillai

et al. 2020

Cells

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Accumulating evidence suggests that neuroinflammation is involved in bipolar disorder (BD) pathogenesis. The tumor necrosis factor-alpha (TNF-α) antagonist infliximab was recently reported to improve depressive symptoms in a subpopulation of individuals with BD and history of childhood maltreatment. To explore the mechanistic mediators of infliximab’s effects, we investigated its engagement with biomarkers of cellular response to inflammation derived from plasma extracellular vesicles enriched for neuronal origin (NEVs). We hypothesized that infliximab, compared to placebo, would decrease TNF-α receptors (TNFRs) and nuclear factor-kappa B (NF-κB) pathway signaling biomarkers, and that history of childhood abuse would moderate infliximab’s effects. We immunocaptured NEVs from plasma samples collected at baseline and at weeks 2, 6, and 12 (endpoint) from 55 participants of this clinical trial and measured NEV biomarkers using immunoassays. A subset of participants (n = 27) also underwent whole-brain magnetic resonance imaging at baseline and endpoint. Childhood physical abuse moderated treatment by time interactions for TNFR1 (χ2 = 9.275, p = 0.026), NF-κB (χ2 = 13.825, p = 0.003), and inhibitor of NF-κB (IκBα)α (χ2 = 7.990, p = 0.046), indicating that higher levels of physical abuse were associated with larger biomarker decreases over time. Moreover, the antidepressant response to infliximab was moderated by TNFR1 (χ2 = 7.997, p = 0.046). In infliximab-treated participants, reductions in TNFR1 levels were associated with improvement of depressive symptoms, an effect not detected in the placebo group. Conversely, reductions in TNFR1 levels were associated with increased global cortical thickness in infliximab- (r = −0.581, p = 0.029), but not placebo-treated, patients (r = 0.196, p = 0.501). In conclusion, we report that NEVs revealed that infliximab engaged the TNFR/NF-κB neuro-inflammatory pathway in individuals with BD, in a childhood trauma-dependent manner, which was associated with clinical response and brain structural changes.

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TNF-α exerts potent anti-rotavirus effects via the activation of classical NF-κB pathway

Cited by 34 publications

References 47 publications

Contribution of glutaredoxin-1 to Fas s-glutathionylation in ethanol-induced liver injury

Contribution of glutaredoxin-1 to Fas s-glutathionylation in ethanol-induced liver injury

Efficient Selection of New Immunobiotic Strains With Antiviral Effects in Local and Distal Mucosal Sites by Using Porcine Intestinal Epitheliocytes

Extracellular Vesicle Biomarkers Reveal Inhibition of Neuroinflammation by Infliximab in Association with Antidepressant Response in Adults with Bipolar Depression

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