Immunosuppressive therapies for inflammatory bowel disease

Zenlea, Talia

doi:10.3748/wjg.v20.i12.3146

Cited by 97 publications

(63 citation statements)

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“…5-aminosalicylic acid, glucocorticoids, immunosuppressants, and infliximab are used for UC treatment. However, several side effects of these agents affect the quality of life of patients, and these drugs cannot produce complete remission in all patients (1)(2)(3)(4)6). Hence, new types of drugs are desired for the treatment of UC.…”

Section: Introductionmentioning

confidence: 97%

“…Colonic tissue samples were fixed in Mildform, then embedded in paraffin before being cut into 4 µm sections, and subjected to histological examination by hematoxylin and eosin staining. Effect of PNU282987 on development of DSS-induced colitis 6. week old ICR mice were treated with 5% DSS for 7 days, and intraperitoneally administered PNU282987 (0.25 mg/kg; n=10, or 0.5 mg/kg; n=13, or 1 mg/kg; n=13) once daily.…”

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confidence: 99%

“…Effect of tropisetron on the level of injury in the mucosa of DSS-treated mice 6. week old ICR mice were treated with 5% DSS for 7 days, and intraperitoneally administered tropisetron (1 mg/kg) once daily.…”

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confidence: 99%

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Involvement of stimulation of α7 nicotinic acetylcholine receptors in the suppressive effect of tropisetron on dextran sulfate sodium-induced colitis in mice

Tasaka

Yasunaga

Kiyoi

et al. 2015

Journal of Pharmacological Sciences

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Ulcerative colitis (UC) involves chronic inflammation of the large intestine. Several agents are used to treat UC, but adverse side effects are remaining problems. We examined the effect of tropisetron as a new type of drug for UC using a dextran sulfate sodium (DSS)-induced model of colitis in mice. We developed a DSS-induced model of colitis and calculated the Disease Activity Index and colon length. We measured myeloperoxidase activity and determined the protein level and mRNA level of cytokines in the colon. DSS-induced colitis was ameliorated by administration of tropisetron and PNU282987. Pre-administration of methyllycaconitine diminished the suppressive effect of tropisetron upon DSS-induced colitis. These findings suggested that α7 nicotinic acetylcholine receptors (α7 nAChRs) were related to the suppressive effect of tropisetron on DSS-induced colitis. Additionally, stimulation of α7 nAChRs decreased the colon level of interleukin-6 and interferon-γ upon DSS administration. Furthermore, stimulation of α7 nAChRs decreased macrophage infiltration, with expression of α7 nAChR increased by DSS administration. These results suggest that the underlying mechanism of this suppressive effect on DSS-induced colitis is via stimulation of α7 nAChRs and involves suppression of expression of pro-inflammatory cytokines. Tropisetron could be a new type of therapeutic agent for UC.

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Section: Introductionmentioning

confidence: 97%

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confidence: 99%

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Involvement of stimulation of α7 nicotinic acetylcholine receptors in the suppressive effect of tropisetron on dextran sulfate sodium-induced colitis in mice

Tasaka

Yasunaga

Kiyoi

et al. 2015

Journal of Pharmacological Sciences

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“…In the present study, we report that xCT is highly expressed in CRC tissues compared with the adjacent normal tissues. Sulfasalazine (SSZ), an anti-inflammatory drug approved for treatment of inflammatory bowel disease and rheumatoid arthritis [19], has exhibited potent inhibition of the cystine transporter xc − and Immunohistochemistry The expression of xCT was detected by immunohistochemical staining on colorectal cancer tissue microarray (Shanghai Outdo Biotech, China) consisting of 88 colorectal carcinoma tissues and their adjacent non-tumorous colorectal tissues. Briefly, the tissue samples were dewaxed in xylene for 20 mins, rehydrated in graded alcohols (100%-95%-75%) for 5 mins each, and then treated with 3% hydrogen peroxide for 30 mins to block endogenous peroxidase activity.…”

Section: Introductionmentioning

confidence: 99%

Xc− inhibitor sulfasalazine sensitizes colorectal cancer to cisplatin by a GSH-dependent mechanism

et al. 2015

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“…Current treatment strategies do not provide a cure and are limited by their inefficacy, toxicity and adverse sideeffects [12][13][14] ; thus necessitating the search for novel therapies. One of the most promising treatments currently being investigated is mesenchymal stem cell (MSC) therapy.…”

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confidence: 99%

Mesenchymal stem cells for the treatment of inflammatory bowel disease: from experimental models to clinical application

Stavely

Sakkal

Stojanovska

et al. 2014

Inflammation and Regeneration

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AustraliaInflammatory Bowel Disease (IBD) is a highly debilitating and potentially fatal idiopathic disorder of the intestinal tract which is exceedingly prevalent in westernized society; however there is concern of an IBD epidemic in Asia due to increasing incidence rates. There is no cure for IBD with current treatments limited by their inefficacy, toxicity and adverse side-effects; thus necessitating the search for novel therapies. In the past decade mesenchymal stem cells (MSCs) have become attractive candidates for the cellular based therapy of IBD. MSCs are easily isolated and expanded from adult bone-marrow and adipose tissue; they possess unique therapeutic characteristics including the ability to home to sites of tissue damage and inflammation, facilitate tissue repair and modulate the immune system. The administration of MSCs in animal models of experimental colitis and clinical trials of fistulising and luminal Crohn's disease have yielded promising results, however an unequivocal therapeutic mechanism remains elusive. This review will explore the clinical application of MSCs in IBD and current evidence from experimental models of colitis elucidating their potential to ameliorate intestinal inflammation.Rec .The cause of IBD is unknown but concordant twin studies have revealed that the development of IBD is likely to require a multi-genetic predisposition and an environmental . The clinical application of MSCs in CD and evidence for the possible mechanisms elucidating their potential to regenerate intestinal epithelium and reduce inflammation in experimental models of colitis will be reviewed. Efficacy of MSCs in Clinical TrialsClinical trials using MSCs for the treatment of CD fistulae and luminal inflammation have demonstrated that MSC therapy in IBD is both efficacious and feasible (summarised in . Furthermore, sustained closure of fistulae has been achieved in 88-100% of subjects 8-12 months after a course of MSC therapy 26,28) ; however these effects are relatively transient given that only 58% of subjects maintain closure after 3 years 29) . This suggests that repeated treatment may be required to maintain the therapeutic benefits of MSC therapy.While autologous and allogeneic AT-MSCs have both demonstrated efficacy in the healing of fistulae, further evidence is required to determine long-term immune tolerance in patients with repeated allogeneic MSC exposure.Bacterial contamination has posed a problem in the expansion of autologous MSCs in the past causing delay in treatment 24,30) . If allogeneic MSCs are determined to be equally efficacious, pre-prepared sources for treatment could prevent such setbacks.One clinical trial has determined that MSCs were as effective in treating fistulae of cryptoglandular origin as they were for fistulae resultant of CD 32,33) . In a study

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Immunosuppressive therapies for inflammatory bowel disease

Cited by 97 publications

References 0 publications

Involvement of stimulation of α7 nicotinic acetylcholine receptors in the suppressive effect of tropisetron on dextran sulfate sodium-induced colitis in mice

Involvement of stimulation of α7 nicotinic acetylcholine receptors in the suppressive effect of tropisetron on dextran sulfate sodium-induced colitis in mice

Xc− inhibitor sulfasalazine sensitizes colorectal cancer to cisplatin by a GSH-dependent mechanism

Mesenchymal stem cells for the treatment of inflammatory bowel disease: from experimental models to clinical application

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