Table 2.

Summary of functional cooperation between MTs and inflammasomes.

Types	Study Results	Exp. Models	Ref.
DNMTs	GA decreased expression of NLRP3, NLRC4, AIM2, and ASC genes in HaCaT cells. GA increased protein expression and activity of DNMT3B in HaCaT cells. GA induced hypermethylation of NLRC4 and ASC gene promoters in HaCaT cells.	Human keratinocytes (HaCaT cells)	[112]
	Mtb infection induced inflammatory responses by increasing NLRP3 gene expression by demethylation of NLRP3 gene promoter in THP-1 cells. NLRP3 promoter activity was decreased by the DNMT Sss I-induced methylation, leading to downregulation of NLRP3 expression in THP-1 cells. Inhibition of NLRP3 promoter methylation by DNMT inhibitor upregulated NLRP3 expression in THP-1 cells.	Human monocytes (HP-1 cells)	[113]
	CPX facilitated accumulation of DNA damage by downregulating the Ogg1 gene expression and induced subsequent NLRP3 inflammasome-activated pyroptosis of the bladder muscle cells in the CPX-treated mice. DNMT1 and DNMT3B methylated Ogg1 gene promoter and promoted Ogg1 gene silencing, resulting in induction of NLRP3 inflammasome-activated inflammatory responses in the bladder muscle cells in the CPX-treated mice. Inhibition of Ogg1 silencing by DNA de-methylation suppressed NLRP3 inflammasome activation and NLRP3 inflammasome-induced inflammatory responses (pyroptosis and IL-1β secretion) in bladder muscle cells.	CPX-treated mice Mouse bladder muscle cells	[114]
	Expression of NLRC4, NLRP12, and IL-1β was increased in KD patients. NLRC4, NLRP12, and IL-1β genes were hypomethylated in KD patients.	White blood cells from KD patients	[115]
	miR-145 decreased plaque formation in vessels of ApoE KO mice. DNMT1 induced hypermethylation of miR-145 promoter and decreased miR-145 expression in vessels of ApoE KO mice. DNMT1-mediated downregulation of miR-145 expression induced NLRP3 inflammasome activation and IL-1β secretion in ApoE KO mice.	ApoE KO mice	[116]
	CtBPs are highly expressed in OA. CtBPs promoted activation of NLRP3 inflammasome, caspase-1, and IL-1β in osteoarthritic cells and OA patients. Expression levels of DNMT1 and DNMT3A were lowered in OA patients. Knockdown of DNMT1 and DNMT3A resulted in hypomethylation of CtBP promoters, leading to CtBP overexpression and NLRP3 inflammasome activation in OA patients.	OA patients Human osteoarthritic cells	[117]
	Melanoma cells treated with TMZ over two months upregulated MGMT expression and became TMZ resistant. TMZ-resistant melanoma cells increased NLRP1 expression and induced NLRP1 inflammasome activation, leading to the maturation and secretion of IL-1β.	Human melanoma cells (1205Lu and HS294T cells)	[118]
	Monocytes derived from chronic heart failure patients carrying DNMT3A mutations revealed a significantly increased expression of inflammasome genes, such as NLRP3 and IL-1β compared with monocytes isolated from chronic heart failure patients with no DNMT3A mutations. DNMT3A silencing in monocytes also increased secretion of pro-inflammatory cytokines. Monocytes of DNMT3A mutation carriers showed increased expression of T-cell-stimulating molecules and changes in T-cell signatures.	Monocytes and T-cells from chronic heart failure patients	[119]
	Ethanol administration induced NLRP3 inflammasome activation, pro-inflammatory cytokine production, and renal inflammation in alcoholic kidneys of mice and HK2 cells. Ethanol administration highly methylated FTO DNA and downregulated FTO expression in alcoholic kidneys of mice and HK2 cells. Inhibition of DNMT1, DNMT3A, and DNMT3B recovered FTO expression and alcohol-induced kidney injury in mice and HK2 cells. FTO promoted PPAR-α m6A methylation and PPAR-α-induced NLRP3 inflammasome activation in alcoholic kidneys of mice and HK2 cells.	Alcohol-induced kidney injury mice Human kidney tubular epithelial cells (HK2 cells)	[120]
Histone MTs	LLO induced NLRP3 inflammasome activation and IL-1β secretion and upregulated NSD1 expression in mouse BMDMs. NSD1 inhibited NLRP3 inflammasome-induced maturation and secretion of IL-1β and IL-18 in LLO-stimulated BMDMs. NSD1 neither restricted NLRP3 inflammasome activation at the chromatin level nor influenced NLRP3 gene expression in LLO-stimulated BMDMs. NSD1 inhibition induced caspase-1 activation and IL-1β secretion in LLO-stimulated BMDMs.	Mouse BMDMs	[127]
	DSS stimulation induced caspase-1 activation and IL-1β secretion in dendritic DC2.4 cells and BMDMs. Inhibition of NLRP12 increased IL-1β secretion in DSS-stimulated dendritic DC2.4 cells and BMDMs. DSS-induced overexpression of Blimp-1 resulted in downregulation of NLRP12 expression in DSS-stimulated DC2.4 cells and BMDMs. TLR4 expression upregulated Blimp-1 expression and leads to Blimp-1-mediated NLRP12 downregulation and IL-1β secretion in DSS-induced colitis mice.	DSS-treated mice Mouse dendritic cells (DC2.4) and BMDMs	[131]
	Contact allergens increased expression of Blimp-1 and IL-18 and decreased NLRP12 expression in NCTC 2544 cells. Blimp-1 silencing increased NLRP12 expression and reduced contact allergen-induced IL-18 production in NCTC 2544 cells.	Human keratinocytes (NCTC 2544 cells)	[133]
	IFI16 interacted with SUV39H1 and GLP generating the IFI16/SUV39H1/GLP complex. IFI16/SUV39H1/GLP complex was recruited to KSHV genome and induced H3K9 methylation during viral infection and latency. The methylated H3K9 served as a docking site for HP1α, resulting in IFI16-mediated epigenetic modification and silencing of KSHV lytic genes.	KSHV-positive PEL cells (BCBL-1 and BC-3 cells) KSHV-negative BJAB cells	[138]