Bacteria of the genus Lactobacillus are Gram-positive microorganisms,belonging to the group of lactic acid bacteria (LAB), natural inhabitants of mammalian gastrointestinal tract. For some LAB strains the probiotic activity has been identified, which means that strains had a beneficial influence on the health of the host.1 Colonization of the intestine by probiotic microorganisms is considered to be an important factor for antagonistic activity against enteropathogens,imodulation of the immune system activity of the host,improved healing of damaged gastric and intestinal mucosa, reducing lactose intolerance or hypocholesterolemic action.2,3 Most of these activities are primarily connected with adherence of the microbial cells to the intestinal mucosa. The surface antigens of bacterial cell, for example, capsular polysaccharides or proteins of the cell wall play the essential role in this process.4 It has been shown that the exopolysaccharides (EPSs) from LAB alter the adhesion of pathogenic bacteria to intestinal mucus.5 There is also a growing number of publications reporting on the use of purified exopolysaccharides as immunostimulatory substances in the experimental therapy.6,7 During the investigations concerning the immunological activity of various polysaccharides from probiotic bacterial strains, the information about the molecular structure of the polysaccharide is essential. While structures of a number of EPSs of LAB are described, they come mainly from the strains of industrial significance.8 In the present work we report the structure of the neutral exopolysaccharide produced by Lactobacillus johnsonii 142, the strain isolated from mice with experimentally induced inflammatory bowel disease (IBD). IBD is a term covering two human diseases with chronic gastrointestinal inflammation: ulcerative colitis and Crohn’s disease, whose pathology is characterized by inflammatory cell infiltration in gut submucosa. The etiology of IBD is largely unknown but it is generally accepted that the chronic inflammation is perpetuated by gut commensal micro- flora in genetically predisposed hosts with altered immune response
to bacterial products.9 Typical IBD changes strongly resembling human disease can be evoked in specific animal models,
mostly in knockout mice colonized with specifically altered gut microflora (Altered Schaedler Flora) containing several species