Table 2.

Some examples of epigenetics coming from training responses in experimental models.

Sample source	Primary stimulus/ disease	Admistration route	Omic platform	Epigenetic change	Localization	Results	Ref.
Infection
Macrophage cultures from bone marrows mice	LPS	Intraperitoneal injection	ChIP-seq	Stable H3K4me1 (24h) Transient H3K27Ac (4h)	Latent enhancer (unmarked in the basal state)	LPS can activate 514 latent enhancers at 4 h and 1,002 at 24 h leading to a short-term transcriptional memory	[65]
Peritoneal macrophages from mice	Candida albicans (β-glucans)	Intraperitoneal injection	Chip-seq	Increase in H3K4me3	Promoters	Protection against reinfection in a monocyte-dependent manner by enhancing dectin-1, C-type lectin receptors, pro-inflammatory cytokines such as TNF-α, IL-6 and IL-18, TLRs and TLR adaptor protein Myd88	[66]
Immune system diseases
Mononuclear cells from mice	arthritis	//	Chip-seq	Elevated levels of phosphorylated H3	Promoters	Upregulation of the AURKA and AURKB genes can lead to promotes proliferation of T lymphocytes. Treatment with the VX-680 attenuated inflammatory reactions and promoted the apoptosis of B cells	[67]
Mouse model of transient hyperglycemia and bovine aortic endothelial cells	Hyperglycemia	//	Chip-seq	Enhanced H3K4 and reduced H3K9 methylation	Promoters	High-glucose-mediated NFKB-p65 gene upregulation that is refractory to glycemic correction	[68]

Abbreviations: AURKA: aurora kinases A; AURKB: aurora kinases B; VX-680; aurora kinase-specific inhibitor.