The Hen or the Egg: Inflammatory Aspects of Murine MPN Models

Table 1

Disease models involving inflammation.

Affected compartment	Cause	Intervention	Phenotype	Reference
	Genetic alteration
Hematopoiesis		TNF-α deletion	Attenuation of MPN development	[28]
Hematopoiesis			Myelofibrosis	[29]
Hematopoiesis		TGF-β inhibition	Restored hematopoiesis, reduced fibrosis	[30]
Hematopoiesis	with	TGF-β inhibition	Restored hematopoiesis	[31]
Hematopoiesis	NFE2 overexpression/mutations		MPN, sAML	[32, 33]
Gastrointestinal mucosa	APC mutations		Colorectal cancer	Reviewed in [34]
Gastrointestinal mucosa	APC^Δ716	COX-2 knockout	Suppression of intestinal polyposis	[35]
Gastrointestinal mucosa	APC^Δ716	PGE2-receptor-2 knockout	Suppression of intestinal polyposis	[36]
Gastrointestinal mucosa	APC^Δ716	Prostaglandin synthase; knockout	Suppression of intestinal polyposis	[37]
Gastrointestinal mucosa	APC^Δ716	15-prostaglandin dehydrogenase (15-PDGH); knockout	Disease exacerbation	[38]
Gastrointestinal mucosa	APC^Δ716	Deletion of either IL-17, IL-6, CCR2, TNFR, or p55	Suppression of intestinal polyposis	[39–42]
	Infectious cause
Hematopoiesis cell intrinsic and extrinsic	TLR activation by bacterial infection		HSC exhaustion	[12]
	Chemical cause
Gastrointestinal mucosa	Azoxymethane (AOM); Dextran Sodium Sulfate (DSS)		Colitis associated colon cancer (CAC)	Reviewed in [34]
Gastrointestinal mucosa	Azoxymethane (AOM)	COX-2 transgene	Increased development of tumors	[43]
Gastrointestinal mucosa	Azoxymethane (AOM); Dextran Sodium Sulfate (DSS)	COX-2 deletion	Increased development of tumors	[44]
Gastrointestinal mucosa	AOM or DSS plus deletion of either IL-17, IL-6, CCR2, TNFR, or p55		Suppression of CAC	[39–42]