The NF- κB pathway is essential for the activation of most inflammatory genes.
Cross-sectional comparisons suggested that lithium and antipsychotic drugs but not conventional antidepressant drugs downregulated expression of most inflammatory genes.
It is conceivable that more inflammatory genes would be up- or down-regulated at the latter compared to the former, as most inflammatory genes are known to act locally.
The quantitative PCR showed a reduction in expression for most inflammatory genes (Wald statistic of p<0.01 indicating a significant treatment effect), with particular reduction in IFNγ of −52% (95% CI −73 to −15, p<0.05); this correlated well with MRI improvements.
Since most inflammatory genes are not directly bound by ALKBH3, we speculate that the inflammatory response may be an indirect consequence of DNA damage accumulation in the ALKBH3 deficient cells [ 24], because DNA damage triggers the activation of inflammatory and other pathways [ 3– 5, 25, 40].
Studies elucidating the effector function of IL-17A or IL-17F on RA synovial cells have reported that while IL-17A and IL-17F may induce similar sets of genes, IL-17A was potent in inducing most inflammatory genes, including IL-6 and G-CSF, in comparison to IL-17F 13, 25.
Interestingly, most inflammatory-related gene expression suppressed (or partially suppressed) by F. tularensis is more associated with viral infection and host antiviral responses, including many known to be induced in response to interferon and/or involved in cell entry of numerous viruses.
CXCL10 was chosen because it was the most highly activated inflammatory gene based on the microarray datasets.
Indeed, no variation in expression was observed for most inflammatory-related genes, while a dramatic increase (280-fold) and a strong decrease (125-fold) were found for MMP-7 and SFRP-1, respectively.
Importantly, it should be noted that in primary microglial cells most of the inflammatory genes were induced stronger than BV-2 cell lines.
