Abstract
BackgroundImiquimod is a Toll-like receptor-7 agonist that regulates immunity and can be used as an immune adjuvant. Ulcerative colitis has a close correlation with immune disorder.AimTo investigate the therapeutic effect of imiquimod on dextran sulfate sodium (DSS)-induced colitis and explore the underlying mechanisms.MethodsC57BL/6J C57 mice received 3% DSS for 7 days to induce ulcerative colitis. Groups of mice were intraperitoneally injected with dexamethasone (DXM, 1.5 mg/kg) or imiquimod (IMQ, 30 mg/kg) at the same time daily. During the experimental period, clinical signs, body weight, stool consistency and visible fecal blood were monitored and recorded daily; colitis was evaluated by disease activity index (DAI) score and by histological score. At the conclusion of the experiment, the level of colonic myeloperoxidase (MPO) activity and the serum levels of the cytokines tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6) and interleukin 10 (IL-10) were measured.ResultsAdministration of 3% DSS for 7 days successfully induced acute colitis associated with diarrhea, bloody mucopurulent stool, body weight decreases, and other changes. Colitis severity was significantly ameliorated in the IMQ treatment groups, as determined by hematoxylin-eosin (HE) staining and histopathological scores. Moreover, IMQ significantly reduced the activity of MPO in colonic tissue and the serum levels of inflammatory cytokines, increased colon length and spleen weight, and effectively inhibited microscopic damage to the colon tissue.ConclusionIMQ had beneficial effects on DSS-induced ulcerative colitis, supporting its further development and clinical application in ulcerative colitis.
Highlights
Ulcerative colitis (UC), whose etiology is not very clear yet, is a chronic, nonspecific inflammatory bowel disease (IBD) whose lesions are mainly limited to the sigmoid colon and the rectal mucosa and submucosa depending on the severity of disease, and it has a chronic and recurrent course [1]
Our experimental studies have shown that IMQ can effectively reduce the clinical symptoms and level of inflammatory mediators in dextran sulfate sodium (DSS)-induced colitis in mice and enhance protective immunity
This study provides experimental evidence to show that IMQ may be a potential drug for the treatment of UC
Summary
Ulcerative colitis (UC), whose etiology is not very clear yet, is a chronic, nonspecific inflammatory bowel disease (IBD) whose lesions are mainly limited to the sigmoid colon and the rectal mucosa and submucosa depending on the severity of disease, and it has a chronic and recurrent course [1]. It has been shown that colonic homeostasis is maintained by the innate immune systems, mainly via Toll-like receptor (TLR) signaling [8, 9]. Counteracting immune disorders can improve the recovery rate, shorten the duration of symptoms, and reduce the complications of UC. This immune approach may offer a new direction for treatment.
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