We find that coculture of human PBMCs with inactivated whole influenza virus (A/Victoria/361/2011) in the presence of very low concentrations of IL-15 results in increased production of myeloid cell-derived cytokines, including IL-12, IFN-α2, GM-CSF, and IL-1β, and an increased frequency of polyfunctional NK cells (defined by the expression of two or more of CD107a, IFN-γ, and CD25).
In cultures stimulated with CMV, EBV, influenza and tetanus peptides, the CD4<sup>+</sup> T-cell count correlated with IL-1β (<i>P </i>=<i> </i>0.045) and CD8<sup>+</sup> T-cell count with IFNγ (<i>P </i>=<i> </i>0.013) and IL-1β (<i>P </i>=<i> </i>0.012).
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.
Furthermore, we show that exogenous IL-1β can drastically alter Th1 responses driven by influenza and lymphocytic choriomeningitis virus infection models and induce IL-17 production.
The frequencies of the IL-1βrs16944 (P = 0.007) and IL-17 rs2275913 (P = 0.006) genotypes were associated with severe influenza disease, while the frequencies of IL-10 rs1800872 and IL-28 rs8099917 were not associated with the disease (P > 0.05).
High Pulmonary Levels of IL-6 and IL-1β in Children with Chronic Suppurative Lung Disease Are Associated with Low Systemic IFN-γ Production in Response to Non-Typeable Haemophilus influenzae.
Thus, the presence of IL1B-31*C allele plus the presence of S. aureus and/or H. influenzae could be related to the development of tonsillitis in this particular Mexican population.
We previously showed that influenza virus M2 or encephalomyocarditis virus (EMCV) 2B proteins stimulate IL-1β secretion following activation of the NLRP3 inflammasome.