Effect of clinical and probiotic Lactobacillus rhamnosus strains on intestinal permeability and bacterial translocation in healthy and colitic rats

Frías, Rafael; Ouwehand, Arthur C.; Spillmann, Thomas; Vankerckhoven, Vanessa; Hewicker‐Trautwein, M.; Salminen, Seppo; Gueimonde, Miguel

doi:10.1016/j.foodres.2009.02.004

Cited by 7 publications

(3 citation statements)

References 22 publications

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“…Colitis was induced by adding 5 % DSS (molecular weight of 37–40 kD; TdB Consultancy, Uppsala, Sweden) to the drinking water, ad libitum for 7 days [ 3 , 4 ].…”

Section: Methodsmentioning

confidence: 99%

“…In both conditions, the inflammatory processes in the gut are associated with disturbances in gastrointestinal motility [ 1 , 2 ]. One animal model of UC involves feeding dextran sulfate sodium (DSS) in drinking water to rodents [ 3 , 4 ]. The model is widely used for screening purposes because of its ease of induction, reproducibility, well-characterized mucosal injury [ 3 ], and its responsiveness to effective agents such as sulfasalazine.…”

Section: Introductionmentioning

confidence: 99%

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STW 5 is effective in dextran sulfate sodium-induced colitis in rats

Wadie

Abdel-Aziz

Zaki

et al. 2012

Int J Colorectal Dis

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PurposeAn herbal preparation, STW 5, used clinically in functional dyspepsia and irritable bowel syndrome, has been shown to possess properties that may render it useful in inflammatory bowel disease (IBD). The present work was conducted to study its effectiveness in a rat model of IBD.MethodsAn experimental model reflecting ulcerative colitis in man was adopted, whereby colitis was induced in Wistar rats by feeding them 5 % dextran sulfate sodium (DSS) in drinking water for one week. STW 5 and sulfasalazine (as a reference standard) were administered orally daily for 1 week before colitis induction and continued during DSS feeding. The animals were then sacrificed, and the severity of colitis was evaluated macroscopically and microscopically. Colon samples were homogenized for determination of reduced glutathione, tumor necrosis factor-α, and cytokine-induced neutrophil chemoattractant-3 as well as myeloperoxidase, glutathione peroxidase, and superoxide dismutase. In addition, colon segments were suspended in an organ bath to test their reactivity towards carbachol, KCl, and trypsin.ResultsSTW 5 and sulfasalazine were both effective in preventing the shortening of colon length and the increase in both colon mass index and total histology score as well as the changes in biochemical parameters measured except changes in dismutase activity. DSS-induced colitis led to marked depression in colonic responsiveness to the agents tested ex vivo, an effect which was normalized by both drugs.ConclusionsThe findings point to a potential usefulness of STW 5 in the clinical setting of ulcerative colitis.

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“…Colitis was induced by adding 5 % DSS (molecular weight of 37–40 kD; TdB Consultancy, Uppsala, Sweden) to the drinking water, ad libitum for 7 days [ 3 , 4 ].…”

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

STW 5 is effective in dextran sulfate sodium-induced colitis in rats

Wadie

Abdel-Aziz

Zaki

et al. 2012

Int J Colorectal Dis

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“…To measure intestinal permeability, an iohexol test was performed on five mice per group essentially as described elsewhere (Frias et al 2009;Frias et al 2014). The test was carried out two weeks before initiation of antibody or PBS injections and again after completion of the 8-day injections.…”

Section: Study Design and Experimental Proceduresmentioning

confidence: 99%

Transglutaminase 2-specific coeliac disease autoantibodies induce morphological changes and signs of inflammation in the small-bowel mucosa of mice

et al. 2016

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Coeliac disease is hallmarked by an abnormal immune reaction against ingested wheat-, rye-and barleyderived gluten and the presence of transglutaminase 2 (TG2)-targeted autoantibodies. The small-bowel mucosal damage characteristic of the disorder develops gradually from normal villus morphology to inflammation and finally to villus atrophy with crypt hyperplasia. Patients with early-stage coeliac disease have TG2-autoantibodies present in serum and small-intestinal mucosa and they may already suffer from abdominal symptoms before the development of villus atrophy. Previously we have shown that intraperitoneal injections of coeliac patient-derived sera or purified immunoglobulin fraction into mice induce a condition mimicking early-stage coeliac disease. In the current study, we sought to establish whether recombinantly produced patient-derived TG2-targeted autoantibodies are by themselves sufficient for the development of such an experimentally induced condition in immune-compromised mice. Interestingly, mice injected with coeliac patient TG2-antibodies had altered small-intestinal mucosal morphology, increased lamina propria cellular infiltration and disease-specific autoantibodies deposited in the small bowel, but did not evince clinical features of the disease. Thus, coeliac patient-derived TG2-specific autoantibodies seem to be sufficient for the induction of subtle small-bowel mucosal alterations in mice, but the development of clinical features probably requires additional factors such as other antibody populations relevant in coeliac disease.

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