Effect of a probiotic Lactobacillus plantarum TN8 strain on trinitrobenzene sulphonic acid‐induced colitis in rats

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The intestine is home to hundreds of different species of microbes. While some of these species are beneficial bacteria that play a crucial role in maintaining gut homeostasis, the others are ‘harmful’ bacteria that may cause various intestinal disorders and diseases, including the inflammatory bowel disease (IBD) (Hooper et al., 2012). The term ‘IBD’ summarizes a group of inflammatory gastrointestinal tract diseases that include ulcerative colitis (UC) and Crohn's disease (CD). IBD refers to an autoimmune disease associated with immunological disorders, genetic susceptibility and microbiological disorders (Packey and Sartor, 2008). The main clinical manifestations include abdominal pain, diarrhoea, fever, clinical signs of bowel obstruction, purulent stools, recurrent attacks, relapses as well as the passage of blood and/or mucus (Baumgart and Sandborn, 2007).
Despite the recent advances and increasing understanding of intestinal inflammation mechanisms, the exact aetiology and pathogenesis of IBD still remain unclear. The use of experimental animal models has provided insights into the complex, multifactorial processes and mechanisms that can result in chronic intestinal inflammation. Chemically induced IBD models, using dextran sulphate sodium (DSS), trinitrobenzene sulphonic acid (TNBS) or oxazolone, are commonly used due to the immediate inflammation, high reproducibility and simplicity of the induction process. As TNBS is a covalently reactive compound, it has often been administered to the animal models to mediate oxidative damage and induce the acute necrosis of the wall of the distal colon, thus making it an ideal model to evaluate the effect of reactive oxygen species (ROS) in IBD. Unlike DSS induction models, TNBS induction is closely similar to human Crohn's disease, as it causes an increase in the Th1/Th2 ratio (De Moreno de LeBlanc and Perdigon, 2010) and regulates the immune cells that are able to inhibit inflammation (Elson and Weaver, 2003).
The anti‐inflammatory potential of a number of probiotics, mostly belonging to the genera of Lactobacillus, has recently been studied in TNBS‐induced colitis models (Lee et al., 2009; Mane et al., 2009). Many studies on probiotic bacterial treatments have reported on promising results, including the reduction in microscopic and biochemical markers of intestinal inflammation (Lee et al., 2009, 2010; Mane et al., 2009). Probiotics have also been investigated for their capacity to reduce the severity of a number of inflammatory conditions, such as pouchitis (Gionchetti et al., 2003) and UC (Venturi et al., 1999).
Probiotics have been described as ‘live micro‐organisms, which, when ingested in sufficient numbers, convey health benefits to the host’ (Ben Salah et al., 2012). They are able to transmit their beneficial effects via a number of mechanisms, including the promotion of crypt cell proliferation and the inhibition of apoptosis (Yan and Polk, 2002), the reduction in pro‐inflammatory cytokine expression (Dieleman et al., 2003; Ben Salah et al., 2012), competition with pathogenic bacteria for mucosal adherence (Dieleman et al., 2003) and the regulation of the intestinal immune system (Dieleman et al., 2003). Accordingly, there has been increasing interest in the search for biologically active probiotic bacterial strains from natural origins for topical administration. The engineering of genetically modified probiotic bacteria and their use as vehicles for the delivery of anti‐inflammatory cytokines or other bioactive molecules has also gained growing momentum in recent years (Steidler et al., 2000).
Of particular interest to the search for bioactive probiotic strains, a previous study using a PBMC model by Ben Salah et al. (2012) has recently reported on a probiotic Lactobacillus plantarum TN8 strain that was found to exhibit encouraging anti‐inflammatory properties in vitro. Strain TN8 induces IL‐10 production and produces small amount of IFN‐γ, IL‐12 and TNF‐α cytokines, with IL‐10/IL‐12 ratios and anti‐inflammatory indices close to standard reference strains (Ben Salah et al., 2012).

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