Dextran sodium sulfate colitis murine model: An indispensable tool for advancing our understanding of inflammatory bowel diseases pathogenesis

Table 1 Factors that influence effectiveness of dextran sodium sulfate to induce colitis

Factors	Variables	Description
DSS	Molecular weight	40-50 kDa for tissue penetration (larger molecule does not penetrate colonic tissue well and smaller molecule has poor distribution)
	Dosage concentration	Ranges from 1.5%-3% used most frequently (1% with mild symptoms and delayed onset)
	Duration of therapy	Acute: 5-10 d administration
	Manufacturer/batch	Chronic: 4-5 repeating cycles of DSS and sterile water
		Various manufacturers with differing potency
Host	Genetically susceptible strain of animal	Certain strains are more susceptible to DSS colitis than other strains.
		Susceptible strains: C3H/HeJ, C57BL/6, BALB/C
Environment	Housing Conditions	Group vs individual unit, frequency of cage changes alters coprophagy by host
	Microbial State	Germ-free vs specific pathogen free vs wild type

DSS: Dextran sodium sulfate.

Table 2 Role of the different classes of mucins in dextran sodium sulfate induced colitis

Mucin gene	Mucin class	Expression site (GI tract)	Chromosome	Pathological findings with DSS treatment	Ref.
Muc1	Membrane bound	All epithelia	3	Muc1-/- protective when challenged with DSS	[64,66]
				Increased thickness with adherent mucus
Muc3	Membrane bound	Intestine, enterocytes	5	Increased up-regulation of Muc3 gene	[65,66]
Muc4	Membrane bound	All epithelia	n.d.	Large type I transmembrane glycoprotein	[65,66,73]
				Muc4-/- more resistant to colitis due to up-regulation of Muc2 due to increase proliferation of cytokines
Muc2	Secretory	Intestine, goblet cells	7	Muc2-/- more susceptible to spontaneous colitis, increased risk of CAC	[66-68]
				DSS produces fulminant colitis vs wild type
Muc5ac	Secretory	Stomach	7		[66]
Muc5b	Secretory	Tongue, sublingual glands	7		[66]

CAC: Colitis-associated cancer; DSS: Dextran sodium sulfate.