Colitis experimental/model

CB2-receptors also exist, in low levels, in cells of the gastrointestinal and cardiovascular system, bone and neuronal cells, liver tissue, and other ceU types [26]. CB2 is up-regulated in inflamed colonic tissue of colitis patients. It is believed that the CB2-receptors are in close interaction with the PPARy-receptor, and both are considered targets for treatment of inflammatory bowel diseases. That was the motivation for Bento et al. [27] to investigate the effect of oral BCP in DSS (dextran sulfate sodium)-induced colitis experimental models. The results showed that BCP inhibited the influx of inflammatory cells. 

Anti-inflammatory testing was performed using the acetic acid colitis rat model described by Fretland (2). Experimental agents were administered 24,16, and 4 hours prior to the 40 second instillation of 3% acetic acid solution in the proximal 6 cm of the colon under light anesthesia. The colon was immediately washed with 5 ml saline and neutrophil inflammation determined by measuring MPO levels in the scraped colonic mucosa. Testing results are provided in Table 2. 

Inflammation leads to changes in permeability of large and polar molecules, which forms the basis of diagnostic tests such as urinary recovery of [51Cr]-EDTA after oral administration. Evidence for increased permeability to very large molecules and small particles in humans is limited, although in an experimental model of colitis in the rat, Lamprecht [83] demonstrated significant uptake of lOOnm-sized particles compared to controls. 

A. Makhlof, Y. Tozuka, and H. Takeuchi, pH-Sensitive nanospheres for colon-specific drug delivery in experimentally induced colitis rat model, Eur. J. Pharm. Biopharm. 72 1-8,2009. 

There is now little doubt that ROMs are produced in excess in patients with aaive IBD. That, at least in experimental colitis, they are rather more than irrelevant epiphenomena is indicated by the anti-inflammatory effect of specific antioxidants. Proof that this is also the case in human disease awaits the outcome of further controlled trials of specific agents interfering with ROM production. Whilst induction of NO production has been shown to occur in association with inflammation and tissue damage in both humans and in animal models, the significance of this is as yet unclear. 

Boirivant, M., Fuss, I.J., Chu, A. and Strober, W. (1998) Oxazolone colitis a murine model of T helper cell type 2 colitis treatable with antibodies to interleukin 4. Journal of Experimental Medicine 188, 1929-1939. 

Investigations performed in rats with experimental acute pancreatitis [196] or ulcerative colitis [197] have shown that both rectal and oral administration of rifaximin decreased colonic bacterial translocation towards mesenteric lymph nodes. In the model of ANP [196] not only was the intra-abdominal spread of enteric bacteria (fig. 8) significantly reduced but also the pancreatic damage was lessened by rifaximin treatment. 

Recent experimental data, coming particularly from animal models of IBD, are consistent with the hypothesis that gut flora and bacterial products are implicated in the initiation and/or perpetuation of chronic intestinal inflammation. Purified bacterial products can initiate and perpetuate experimental colitis [1,2]. 

Based on the experimental observation of a beneficial effect of intracolonic amoxicillin-clavulanic acid in a rat model of colitis, Casellas et al. [33] used an enteric-coated amoxicillin-clavulanic acid (1 g amoxicillin plus 250 mg clavulanic acid, t.i.d.) in active UC. They also evaluated the release of inflammatory mediators (IL-8, TXB2, PGE2) in rectal dialysates. After short-term treatment, this formulation decreased intraluminal release of IL-8 and other inflammatory mediators and led to an improvement of patients with active UC. 

HV146 Kanauchi O., T. Iwanaga, K. Mitsu-yama, et al. Butyrate from bacterial fermentation of germinated barley foodstuff preserves intestinal barrier function in experimental colitis in the rat model. J Gastroenterol Hepatol 1999 14(9) 880-888. 

Groux et al. [90] showed that human and mouse CD4+ T cells chronically activated in the presence of IL-10 in vitro were anergic. These cells suppressed T cell proliferation in vitro in a cell contact-independent way by producing the immunosuppressive cytokines IL-10 and TGF-p,. Further, the cells also suppressed the development of experimental colitis in a mouse model [90]. These suppressive cells were denoted T regulatory type 1 cells (Trl). 

Zurita-Turk, M., Del Carmen, S., Santos, A.C., et al. (2014) Lactococcus lactis carrying the pValac DNA expression vector coding for IL-10 reduces inflammation in a murine model of experimental colitis. BMC Biotechnol 14, 73. 

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