Furthermore, (+)‑pinoresinol‑O‑β‑D‑glucopyranoside exhibited pronounced inhibitory effects on the expression of influenza H1N1 virus‑induced pro‑inflammatory mediators, including tumor necrosis factor‑α, interleukin (IL)‑6, IL‑8 and monocyte chemoattractant protein 1.
Influenza vaccine responses to all subunit strains (H1N1, H3N2, B strain) were preserved with methotrexate (MTX) and tumor necrosis factor inhibitor (TNFi) drug exposure.
Previously, we showed that an oligodeoxynucleotide with AAAG repeats (AAAG ODN) rescued mice from fatal acute lung injury (ALI) induced by influenza virus and inhibited production of tumor necrosis factor-α (TNF-α) in the injured lungs.
It was found that ethanol and water crude extracts of C. longa and K. parviflora induced significant upregulation of TNF-α and IFN-β mRNA expressions, suggesting their roles in the inhibition of H5N1 virus replication.
Two compounds that showed great anti-inflammatory activity were isolated from C. paniculatum and elucidated as cynanversicoside A and cynanversicoside C. Cytokine assay demonstrated that cynanversicoside A and cynanversicoside C can suppress the production of TNF-α, IL-6 and IL-1β in Mice Pulmonary Microvascular Endothelial Cells (MPMEC) after Influenza virus A/FM/1/47 infection (p < .05) and also decreased the expressions of p-p65 and p-IκBα in infected cells.
Elevated sputum concentrations of IL-1β, IL-10, and tumor necrosis factor (TNF)-α were detected in samples qPCR positive for either H influenzae or M catarrhalis.
Influenza was associated with overexpression of 20 genes, including those encoding the cytokines tumor necrosis factor and IL-12; the kinases MEK, TBK-1, and STAT-1; the apoptosis proteins caspase-8 and caspase-10; the influenza double-stranded RNA receptor RIG-I and its downstream effector MAVS; and pyrin, an IFN-stimulated protein involved in influenza resistance.
The expression of IL-2, IL-6, IFN-γ, TNF-α in the patients with influenza H1N1 2009 infection was significantly increased; while IL-10 expression decreased and IL-4 expression did not change.
Influenza-specific memory CD8(+) T-cell response maintained a highly functional profile in terms of multitude of effector molecule expression (CD107a, IFN-γ, TNF-α, MIP-1β and IL-2) and showed high avidity even in the setting of SIV infection.
Human airway epithelial cells were infected with influenza and TNF-α concentration in supernatant was measured before supernatant was applied to human neuroblastoma cells.
We compared the prevalence of 8 polymorphisms in the tumor necrosis factor and mannose-binding lectin genes among 105 children and young adults with fatal influenza with US population estimates and determined in subanalyses whether these polymorphisms were associated with sudden death and bacterial co-infection among persons with fatal influenza.
In comparison with human seasonal influenza (H1N1) viruses, clade 1, 2.1, and 2.2 H5N1 viruses induced higher levels of tumor necrosis factor-alpha in primary human macrophages.
The treatment induced expression of the inflammatory cytokines IL-6 and TNF in bronchoalveolar lavage fluid 8- and 40-fold greater, respectively, than that caused by lethal influenza infection.
While wild-type mice induced tumor necrosis factor-a (TNF) after non-typeable H. influenzae challenge, TLR2(-/-) and TLR4(-/-) mice lack TNF induction in the early phase of otitis media.
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.