Table 2.

Differences of histone modification between different methods induced sepsis.

Sepsis model	Histone site	Regulatory enzymes	Effects	ref
LPS stimulation	H3K4me3	SET1	Recruited SET1 upregulates H3K4me3 on promoter regions of p65 target genes and modulates inflammatory response.	[39]
		SYMD1	SYMD1 promotes H3K4me3 and increases IL-6 release in endothelial cells.	[40]
	H3K4me1		Upregulation of H3K4me1 promotes IFN-γ expression and mediates the generation of memory-like NK cells.	[113]
	H3K4/9me2		H3K4/9me2 demethylation regulates LSD1-BCL2L11/DUSP2 signaling and further limits IL-1β production.	[100]
	H3K27me3	JMJD3	JMJD3-induced H3K27me3 demethylation acts as a pro-inflammatory factor.	[42–44]
	H3k36me3		H3k36me3 promotes pro-inflammatory macrophage and enhances IL-1β production.	[99]
	H4K16ac	SIRT1	SIRT1 reduces H3K16 acetylation and inhibits TNF-α transcription during sepsis-induced inflammation.	[55]
	Histone3ac		The increased acetylated histones promoted the progression of sepsis by upregulating microRNA-29a to inhibit STAT3.	[57]
		HDACs	HDACs catalyzes the deacetylation of histone H3, which enables the activity of PAD4 and the formation of NETosis.	[109]
	H3K18Kla	p300	H3K18Kla promotes macrophage alternation from M1-like phenotype to M2-like.	[9]
Bacterial infection intraperitoneally	H3K27me3	JMJD3	H3K27me3 demethylation enhances pro-inflammatory cytokine IL-1β production as well as IL-6, TNF-α, and MCP-1 expression.	[43]
Cecal ligation and puncture (CLP)	H3K4/27me		Decreased H3K4me and upregulated H3K27me on GATA3 and TBX21 promotes CD4 + T cell inactivation and dysfunction.	[113]
	Histone ac	HDAC6	HDAC6-induced histone deacetylation might reduce B lymphocyte percentage.	[121]

Methyltransferases MLL1, SYMD1, Demethylase JMJD1, Acetyltransferases p300, Deacetylases HDACs, SIRT1.