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Discovery of a Novel Multi-Strains Probiotic Formulation with Improved Efficacy toward Intestinal Inflammation.

ABSTRACT: Dysbiosis is commonly detected in patients with inflammatory bowel disease (IBD), supporting the concept that a dysregulated immune reaction to bacterial antigens has a pathogenic role in the development of intestinal inflammation. In the present study, we have investigated the beneficial effects of a novel probiotic formulation assembled by combining four probiotics (Streptococcus thermophilus, Lactobacillus casei, Bifidobacterium breve) with Bacillus subtilis, a Gram-positive bacterium, with extensive bio-applications. Mice rendered colitic by administration of TNBS or DSS were administered with Bacillus subtilis alone, Vivomixx® or the novel Five strains formulation. Vivomixx® attenuated the severity of inflammation and reduced the development of signs and symptoms of colitis in both models. Adding Bacillus subtilis to Vivomixx® improved the beneficial effects of the bacterial therapy. The novel Five strains formulation was as effective as Vivomixx® in reducing the development of signs and symptoms of colitis and reduced the expression of pro-inflammatory mediators including Il-6 and Tnf-? while increased the expression of Il-10 mRNA and the number of Treg. In summary, we have shown that a novel Five strains probiotics formulation exerts beneficial effects on two chemical models of colitis, establishing Bacillus subtilis as a probiotic in rodent models of inflammation.

SUBMITTER: Biagioli M

PROVIDER: S-EPMC7400193 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature

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Discovery of a Novel Multi-Strains Probiotic Formulation with Improved Efficacy toward Intestinal Inflammation.

Biagioli Michele M Carino Adriana A Di Giorgio Cristina C Marchianò Silvia S Bordoni Martina M Roselli Rosalinda R Distrutti Eleonora E Fiorucci Stefano S

Nutrients 20200630 7

Dysbiosis is commonly detected in patients with inflammatory bowel disease (IBD), supporting the concept that a dysregulated immune reaction to bacterial antigens has a pathogenic role in the development of intestinal inflammation. In the present study, we have investigated the beneficial effects of a novel probiotic formulation assembled by combining four probiotics (Streptococcus thermophilus, Lactobacillus casei, Bifidobacterium breve) with Bacillus subtilis, a Gra ...[more]

PMID: 32629887

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Project description:Lactobacillus reuteri (L. reuteri) is a probiotic that inhibits the severity of enteric infections and modulates the immune system. Human-derived L. reuteri strains DSM17938, ATCC PTA4659, ATCC PTA 5289, and ATCC PTA 6475 have demonstrated strain-specific immunomodulation in cultured monocytoid cells, but information about how these strains affect inflammation in intestinal epithelium is limited. We determined the effects of the four different L. reuteri strains on lipopolysaccharide (LPS)-induced inflammation in small intestinal epithelial cells and in the ileum of newborn rats. IPEC-J2 cells (derived from the jejunal epithelium of a neonatal piglet) and IEC-6 cells (derived from the rat crypt) were treated with L. reuteri. Newborn rat pups were gavaged cow milk formula supplemented with L. reuteri strains in the presence or absence of LPS. Protein and mRNA levels of cytokines and histological changes were measured. We demonstrate that even though one L. reuteri strain (DSM 17938) did not inhibit LPS-induced IL-8 production in cultured intestinal cells, all strains significantly reduced intestinal mucosal levels of KC/GRO (∼IL-8) and IFN-γ when newborn rat pups were fed formula containing LPS ± L. reuteri. Intestinal histological damage produced by LPS plus cow milk formula was also significantly reduced by all four strains. Cow milk formula feeding (without LPS) produced mild gut inflammation, evidenced by elevated mucosal IFN-γ and IL-13 levels, a process that could be suppressed by strain 17938. Other cytokines and chemokines were variably affected by the different strains, and there was no toxic effect of L. reuteri on intestinal cells or mucosa. In conclusion, L. reuteri strains differentially modulate LPS-induced inflammation. Probiotic interactions with both epithelial and nonepithelial cells in vivo must be instrumental in modulating intrinsic anti-inflammatory effects in the intestine. We suggest that the terms anti- and proinflammatory be used only to describe the effects of a probiotic in the living host.

Project description:Probiotics and commensal intestinal microbes suppress mammalian cytokine production and intestinal inflammation in various experimental model systems. Limited information exists regarding potential mechanisms of probiotic-mediated immunomodulation in vivo. In this report, we demonstrate that specific probiotic strains of Lactobacillus reuteri suppress intestinal inflammation in a trinitrobenzene sulfonic acid (TNBS)-induced mouse colitis model. Only strains that possess the hdc gene cluster, including the histidine decarboxylase and histidine-histamine antiporter genes, can suppress colitis and mucosal cytokine (interleukin-6 [IL-6] and IL-1? in the colon) gene expression. Suppression of acute colitis in mice was documented by diminished weight loss, colonic injury, serum amyloid A (SAA) protein concentrations, and reduced uptake of [(18)F]fluorodeoxyglucose ([(18)F]FDG) in the colon by positron emission tomography (PET). The ability of probiotic L. reuteri to suppress colitis depends on the presence of a bacterial histidine decarboxylase gene(s) in the intestinal microbiome, consumption of a histidine-containing diet, and signaling via the histamine H2 receptor (H2R). Collectively, luminal conversion of l-histidine to histamine by hdc(+) L. reuteri activates H2R, and H2R signaling results in suppression of acute inflammation within the mouse colon.Probiotics are microorganisms that when administered in adequate amounts confer beneficial effects on the host. Supplementation with probiotic strains was shown to suppress intestinal inflammation in patients with inflammatory bowel disease and in rodent colitis models. However, the mechanisms of probiosis are not clear. Our current studies suggest that supplementation with hdc(+) L. reuteri, which can convert l-histidine to histamine in the gut, resulted in suppression of colonic inflammation. These findings link luminal conversion of dietary components (amino acid metabolism) by gut microbes and probiotic-mediated suppression of colonic inflammation. The effective combination of diet, gut bacteria, and host receptor-mediated signaling may result in opportunities for therapeutic microbiology and provide clues for discovery and development of next-generation probiotics.

Dataset Information

Discovery of a Novel Multi-Strains Probiotic Formulation with Improved Efficacy toward Intestinal Inflammation.

Publications

Discovery of a Novel Multi-Strains Probiotic Formulation with Improved Efficacy toward Intestinal Inflammation.

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