Abstract
Innate immune response induces positive inflammatory transducers and regulators in order to attack pathogens, while simultaneously negative signaling regulators are transcribed to maintain innate immune homeostasis and to avoid persistent inflammatory immune responses. The gene expression of many of these regulators is controlled by different epigenetic modifications. The remarkable impact of epigenetic changes in inducing or suppressing inflammatory signaling is being increasingly recognized. Several studies have highlighted the interplay of histone modification, DNA methylation, and post-transcriptional miRNA-mediated modifications in inflammatory diseases, and inflammation-mediated tumorigenesis. Targeting these epigenetic alterations affords the opportunity of attenuating different inflammatory dysregulations. In this regard, many studies have identified the significant anti-inflammatory properties of distinct naturally-derived phytochemicals, and revealed their regulatory capacity. In the current review, we demonstrate the signaling cascade during the immune response and the epigenetic modifications that take place during inflammation. Moreover, we also provide an updated overview of phytochemicals that target these mechanisms in macrophages and other experimental models, and go on to illustrate the effects of these phytochemicals in regulating epigenetic mechanisms and attenuating aberrant inflammation.
Highlights
The innate immune system is the non-specific, inherited immune defense mechanism encoded in the germ-line genes of the host [1]
This report covered different phytochemicals used in distinct inflammatory experimental models and focused, in particular, on their epigenetic regulatory mechanisms, few studies have translated the epigenetic-mediated actions of these plant derivatives to human models and little is understood about gene regulation mediated by natural products in health and disease [27]
It will be of great benefit if future research is directed to revealing the most effective phytochemicals in attenuating inflammatoryassociated dysregulations, neurodegenerative and cardiovascular diseases
Summary
The innate immune system is the non-specific, inherited immune defense mechanism encoded in the germ-line genes of the host [1]. Through epigenetic mechanisms (Table 1 and Figure 3), RES attenuated LPS-mediated inflammation in RAW264.7 macrophages through downregulating miR-155 and concurrently boosting, SOCS1 expression, leading to the inhibition of the inflammatory factors, TNF-a, IL-6, MAPKs [149]. It inhibits TLR4 and MyD88 expression in activated RAW 264.7 macrophages [142, 143] It inhibits NF-kB, MAPK, IRF-3 and AP-1 transcription factors, as well as, iNOS, COX-2, and 5-LOX enzymes [124, 143,144,145,146,147] It reduces NF-kB induced proinflammatory cytokines, including TNF-a, IL-6, and IL-1b, and the free radicals, NO and ROS, and LTs and PGs levels [124, 132, 140, 142, 147,148]. Similar to SFN, CA inhibits LPS-induced TLR4 receptor oligomerization and activates Nrf pathway [298, 299] (Table 1 and Figure 1)
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