Table 1.

The different types of animal model induced through various methods are summarized with their implication and role in IBD pathogenesis ([52,162]) (the generation of different genetically engineered mice are reviewed in detailed in [162,163]).

Sr. No.	Group	Animal Model	Information
1.	Chemically Induced	Acetic acid (rat)	Reduced inflammation and myeloperoxidase activity (MPO) activity, restoration of contraction of isolated colon. Conclusion: Cyclo-oxygenase (COX) and lipo-oxygenase-mediated proinflammatory products mediated IBD pathogenesis.
		DSS	CD4+ T-cell transfer colitis model (Rag−/−) and acute DSS-induced IBD used for identifying the function of Foxp3+ Tregs. Conclusion: Isolated CD4+ T-cells from Foxp3+ Tregs-depleted mice secrete IL-13, IL-17A, and IFN-γ with severe IBD. Foxp3+ Tregs establish mucosal homeostasis, a therapeutic option for patients with IBD.
		TNBS	Depletes colon-specific Foxp3+ Tregs but with no effect on spleen, mesenteric lymph nodes, and ileum. Higher expression of Fas ligand in colitis mice; no depletion of colon-specific Tregs in DNBs-induced colitis in Fas−/− deficient mice. Conclusion: Fas/FasL pathway mediates depletion of Foxp3+ Tregs in the colon.
		Oxazolon	Experimental colitis induced in SJL/J mice. Th2-driven production of IL-4 and IL-5. Conclusion: Higher similarity with human UC, and Th2 response helps better understand UC.
		PG/PS polymer (Peptidoglycan polysaccharide)	Elevates plasma nitrite and nitrate levels, higher colonic mucosal permeability, and MPO activity. Conclusion: PG-PS induces chronic colitis in rats confirmed by higher NO production.
		Auer	Experimental colitis was induced by Auer with increased vascular permeability. Conclusion: Induced colitis helps better understand the injury mechanism as well as the pathogenic mechanism.
		Carrageenan (CGN)	Degrades CGN, induces ulcers in mice, rats, rabbits, and guinea-pigs. Changes spleen lymphocytes activity, suppresses immune system to cause IBD. Conclusion: CGN-based colitis follows the NF-κB signalling pathway, upregulate TNF-α and ICAM-1.
		Indomethacin	Inhibition of prostaglandin E1 and E2. Conclusion: Higher production of reactive oxygen species (ROS) and other free radicals, as well as apoptosis mediated by caspase-3, which causes IBD.
2.	Adaptive Cell Transfer	CD45RB	Naïve and memory CD4+ T-cell populations (Th1 and Th2 clone) are included in CD45RBhigh and CD45RBlow fractions. Adoptively transferred CD4+ CD45RBhigh T-cells extracted to SCID mice from wild-type mice developed colitis in 6 to 12 weeks. Conclusion: It helps unravel earlier immune–inflammation events.
		ECOVA	BALB/c and SCID mice received CD4 T-cells purified from Rag−/− mice crossed to Tg mice expressing ovalbumin (ova)-specific TCR. Conclusion: Predominant production of IL-4 in the early stage and IL-10 in the later stage in ova-specific CD4 T-cells was observed. Additionally, co-transfer of IL-10 secreting ova-specific CD4 T-cells prevented the development of colitis, and expanded ova-specific CD4 T-cells induced lymphadenopathy and caused colitis.
		CD8 Transfer	DNBS causes colitis, IFN-γ-producing cytotoxic CD8+ T-cell (Tc1) recruitment. Colitis was prevented by the antibody depletion of CD8+ and not with CD4+ T-cells. Conclusion: Relapse of colitis in normal mice with Ag-specific CD8 T-cells reveals TC1′s role in intestinal inflammation.
3.	Bacteria-Infected Model	Citrobacter rodentium	Model for human infectious colitis induced by E. coli. Transfer of CD4+ T-cells induced the secretion of IFN-γ, IL-17, IL-2 and ameliorates the activity of IL-10. Conclusion: CD4+ population generated in C. rodentium infection mice renders protection to the non-infected recipient via Th1-induced species-specific immune response (mainly IL-17), elevated secretion of systemic IgG, and fecal IgA.
		Helicobactor hepaticus	Homozygous SCID mice (with CD45RB cells) infected with H. hepaticus and CD4+ CD45RBhigh T-cells. Conclusion: Allows the investigation of abnormal immune response and disease.
4.	Conogenic Model	C3H/HeJBir	C3H/HeJBir (C3Bir) mice cause a missense mutation in the third exon of the Tlr4 gene, resulting in the spontaneous development of inflammation in the colon and cecum. Conclusion: Helpful in understanding the immune system and formal genetic studies of the disease.
		SAMP1/Yit	A new senescence-accelerated mouse (SAM) P1/Yit strain was established that spontaneously developed enteric inflammation under specific pathogen-free conditions. Develops CD-like ileitis, with higher levels of IFN-γ and TNF-α. Inflated levels of IL-13 and IL-5 point out the role of Th2 in causing chronic inflammation. Conclusion: Validates the role and interaction of gut microbiota in IBD pathogenesis.
		SAMP1/YitFc	Developed by mating brother–sister for over 20 generations. Conclusion: Ileitis was developed at the earlier age of 10 weeks. Useful in understanding the chronic pathological conditions of CD to help design novel therapeutic regimens.
5.	Spontaneous	Cotton-top tamarin	Small unique primate group that develops spontaneous colitis, similar to human UC. Develops secondary complications of sclerosing cholangitis, colon-based adenocarcinoma, and elevated fecal TNF-α, seen in human UC. Conclusion: Role of anti-TNF-α in human UC under investigation.