Abstract
In inflammatory bowel disease (IBD), experimental models have proven to be important tools for evaluating potential therapeutic agents and for investigating the mechanisms of pathogenesis. Oxidative stress and the immune response have been associated with acetic acid (AA)-induced ulcerative colitis (UC). Our study aimed to evaluate, for the first time, the ability of a spore-based probiotic and an amino acid and immunoglobulin supplement in reducing tissue damage and inflammatory responses in an experimental animal model of UC. Forty-two Wistar rats were divided into six groups, receiving 1% carboxymethylcellulose, 4% AA, MegaSporeBiotic™ (MSB; 1 × 109 colony forming units/day) and MegaMucosa™ (MM; 70 mg/100 g/day). Pretreatment with MSB or MM alone and in combination significantly lowered inflammation and reduced damage to the colonic mucosa. Pretreatment with these agents resulted in levels of proinflammatory cytokines, vascular tight junction proteins, and measures of oxidative stress similar to those reported for methylprednisolone, one of the first-line therapies for moderate to severe activity of UC. The protection was further confirmed by histologic analysis of the colon tissue. In conclusion, pretreatment with probiotic spore-forming Bacillus strains and a supplement of amino acids in combination with immunoglobulins exhibited anti-inflammatory and antioxidant effects in an AA-induced rat model of UC.
Highlights
Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD), with an ever-increasing incidence and prevalence worldwide [1]
tumor necrosis factor (TNF)-α levels were significantly higher compared with the healthy control group
Even if the number of Bacillus is lower compared to Lactobacillus or Bifidobacteria species, it should be clear that Bacillus species, for example B. subtillis, have an important role in the lymphoid tissue associated with the intestine
Summary
Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD), with an ever-increasing incidence and prevalence worldwide [1]. The disease poses particular concern due to an increased risk for patients with UC to develop colorectal cancer [2]. The release of inflammatory mediators such as cytokines and arachidonic acid metabolites, as well as free radicals, results in oxidative damage to the colonic tissue [6,7]. GCs act on local bowel inflammation by reducing local cytokine and reactive oxygen species (ROS) production, limiting tissue damage [8]. This treatment often results in detrimental side effects, including severe and life-threatening infections [9]
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