Lactobacillus fermentum, a probiotic capable to release glutathione, prevents colonic inflammation in the TNBS model of rat colitis.
OBJECTIVE
Inflammatory bowel disease is associated with intestinal oxidative stress. In the present study we test the preventative effect of Lactobacillus fermentum, a probiotic that produces per se glutathione, in the trinitrobenzenesulphonic acid (TNBS) model of rat colitis.


METHODS
Colitis was induced in rats by intracolonic administration of 10 mg of TNBS dissolved in 0.25 ml of 50% ethanol. L. fermentum was administered orally (5x10(8) CFU suspended in 0.5 ml of skim milk) to a group of rats for 3 weeks, starting 2 weeks before colitis induction. Colonic damage was evaluated both histologically and biochemically, and the colonic luminal contents were used for bacterial studies as well as for short chain fatty acid (SCFA) production.


RESULTS
L. fermentum treatment resulted in an amelioration of the inflammatory response in colitic rats as evidenced histologically and by a significant reduction of colonic MPO activity (P<0.05). The probiotic partially counteracted the colonic glutathione depletion induced by the inflammatory process. In addition, probiotic-treated colitic rats showed significant lower colonic tumour necrosis factor (TNF)alpha levels (P<0.01) and inducible nitric oxide synthase (iNOS) expression when compared to non-treated rats. Finally, the probiotic induced growth of Lactobacilli species and production of SCFA in colonic contents in comparison with control colitic rats.


CONCLUSIONS
Administration of the probiotic L. fermentum facilitates the recovery of the inflamed tissue in the TNBS model of rat colitis, an effect associated with increased levels of glutathione as well as with amelioration of the production of some of the mediators involved in the inflammatory response of the intestine, such as TNFalpha and NO.
Peran
Laura
L
Department of Pharmacology, School of Pharmacy, University of Granada, Campus Universitario La Cartuja s/n, 18071 Granada, Spain.
Camuesco
Desiree
D
Comalada
Monica
M
Nieto
Ana
A
Concha
Angel
A
Adrio
José Luis
JL
Olivares
Mónica
M
Xaus
Jordi
J
Zarzuelo
Antonio
A
Galvez
Julio
J
D000704:Analysis of Variance; D000818:Animals; D003092:Colitis / Q000139:chemically induced / Q000382:microbiology / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D015169:Colony Count, Microbial; D004195:Disease Models, Animal; D005232:Fatty Acids, Volatile / Q000096:biosynthesis; D005260:Female; D005978:Glutathione / Q000187:drug effects* / Q000378:metabolism*; D018836:Inflammation Mediators / Q000378:metabolism; D007413:Intestinal Mucosa / Q000378:metabolism / Q000382:microbiology / Q000473:pathology / Q000503:physiopathology; D052197:Limosilactobacillus fermentum / Q000302:isolation & purification; D007975:Leukotriene B4 / Q000378:metabolism; D020556:Neutrophil Infiltration / Q000187:drug effects; D052247:Nitric Oxide Synthase Type II / Q000096:biosynthesis / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects; D009195:Peroxidase / Q000187:drug effects / Q000378:metabolism; D019936:Probiotics / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D014302:Trinitrobenzenesulfonic Acid; D014409:Tumor Necrosis Factor-alpha / Q000187:drug effects / Q000378:metabolism
D005232:Fatty Acids, Volatile; D018836:Inflammation Mediators; D014409:Tumor Necrosis Factor-alpha; D007975:Leukotriene B4; D014302:Trinitrobenzenesulfonic Acid; D009195:Peroxidase; D052247:Nitric Oxide Synthase Type II; D005978:Glutathione