<i>Bifidobacterium lactis</i>attenuates onset of inflammation in a murine model of colitis

Philippe, David; Favre, Laurent; Foata, Francis; Adolfsson, Oskar; Perruisseau-Carrier, G; Vidal, Karine; Reuteler, Gloria; Dayer-Schneider, Johanna; Mueller, Christoph; Blum, Stéphanie

doi:10.3748/wjg.v17.i4.459

Cited by 54 publications

(33 citation statements)

References 62 publications

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“…1A). This was not unexpected for B. animalis I-2494, because this probiotic species has antiinflammatory activities in various animal models (14,15). However, in our experiments, the L. lactis I-1631 FMP was highly effective in reducing colitis (Fig.…”

Section: Resultscontrasting

confidence: 49%

Host lysozyme-mediated lysis of Lactococcus lactis facilitates delivery of colitis-attenuating superoxide dismutase to inflamed colons

Ballal

Veiga

Fenn

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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Beneficial microbes that target molecules and pathways, such as oxidative stress, which can negatively affect both host and microbiota, may hold promise as an inflammatory bowel disease therapy. Prior work showed that a five-strain fermented milk product (FMP) improved colitis in T-bet−/−Rag2−/− mice. By varying the number of strains used in the FMP, we found that Lactococcus lactis I-1631 was sufficient to ameliorate colitis. Using comparative genomic analyses, we identified genes unique to L. lactis I-1631 involved in oxygen respiration. Respiration of oxygen results in reactive oxygen species (ROS) generation. Also, ROS are produced at high levels during intestinal inflammation and cause tissue damage. L. lactis I-1631 possesses genes encoding enzymes that detoxify ROS, such as superoxide dismutase (SodA). Thus, we hypothesized that lactococcal SodA played a role in attenuating colitis. Inactivation of the sodA gene abolished L. lactis I-1631’s beneficial effect in the T-bet−/−Rag2−/− model. Similar effects were obtained in two additional colonic inflammation models, Il10−/− mice and dextran sulfate sodium-treated mice. Efforts to understand how a lipophobic superoxide anion (O2−) can be detoxified by cytoplasmic lactoccocal SodA led to the finding that host antimicrobial-mediated lysis is a prerequisite for SodA release and SodA’s extracytoplasmic O2− scavenging. L. lactis I-1631 may represent a promising vehicle to deliver antioxidant, colitis-attenuating SodA to the inflamed intestinal mucosa, and host antimicrobials may play a critical role in mediating SodA’s bioaccessibility.

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Section: Resultscontrasting

confidence: 49%

Host lysozyme-mediated lysis of Lactococcus lactis facilitates delivery of colitis-attenuating superoxide dismutase to inflamed colons

Ballal

Veiga

Fenn

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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“…Bifidobacterium was significantly decreased in children who developed autoimmunity but had not progressed to T1D (7). The levels of Bifidobacterium have been related to improved glucose metabolism, insulin resistance, and low-grade inflammation (55,56). Given the relationship between bacteriophages and bacterial hosts, it is conceivable that the changes in bacteriophages before seroconversion modulate bacterial abundance and eventually lead to overt bacteria dysbiosis.…”

Section: Discussionmentioning

confidence: 99%

Intestinal virome changes precede autoimmunity in type I diabetes-susceptible children

Zhao

Vatanen

Droit

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

251

240

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Viruses have long been considered potential triggers of autoimmune diseases. Here we defined the intestinal virome from birth to the development of autoimmunity in children at risk for type 1 diabetes (T1D). A total of 220 virus-enriched preparations from serially collected fecal samples from 11 children (cases) who developed serum autoantibodies associated with T1D (of whom five developed clinical T1D) were compared with samples from controls. Intestinal viromes of case subjects were less diverse than those of controls. Among eukaryotic viruses, we identified significant enrichment ofCircoviridae-related sequences in samples from controls in comparison with cases. Enterovirus, kobuvirus, parechovirus, parvovirus, and rotavirus sequences were frequently detected but were not associated with autoimmunity. For bacteriophages, we found higher Shannon diversity and richness in controls compared with cases and observed that changes in the intestinal virome over time differed between cases and controls. Using Random Forests analysis, we identified disease-associated viral bacteriophage contigs after subtraction of age-associated contigs. These disease-associated contigs were statistically linked to specific components of the bacterial microbiome. Thus, changes in the intestinal virome preceded autoimmunity in this cohort. Specific components of the virome were both directly and inversely associated with the development of human autoimmune disease.

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“…Bifidobacteria had beneficial effect in both animal models [160] and in patients with UC and CD [161][162][163], while lower count of Bifidobacteria was measured in IBD [147]. One potential protective mechanism is the activation of Tregs, as it has been observed in the case of Clostridia and B. fragilis (see above).…”

Section: The Microbiotamentioning

confidence: 95%

“…The probiotic Bifidobacterium breve induced IL-10-producing Treg type 1 cells by activating intestinal CD103+ dendritic cells via the TLR2/MyD88 pathway [164]. Another strain, Bifidobacterium lactis significantly decreased the colonic expression of various pro-inflammatory, dendritic and T-cell markers, like IL-6, TNF-, COX-2, CD40-L or IFN-in mice [160].…”

Section: The Microbiotamentioning

confidence: 99%

Gut Inflammation: Current Update on Pathophysiology, Molecular Mechanism and Pharmacological Treatment Modalities

Gyires¹,

Tóth²,

Zádori

2014

CPD

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Inflammatory bowel disease (IBD) is a chronic and relapsing inflammatory condition of the gastrointestinal tract. The two main forms of IBD are Crohn's disease and ulcerative colitis. According to the recent concept the disease is caused by a combination of factors, including genetics, immune dysregulation, barrier dysfunction and the change in microbial flora. Environmental factors, such as changes in diet, antibiotic use, smoking or improved domestic hygiene (e.g. eradication of intestinal helminths) probably contribute to the development and increased prevalence of IBD. Dysregulation of mucosal immunity in IBD causes an overproduction of inflammatory cytokines which resulted in uncontrolled intestinal inflammation. Based on extensive research over the last decade, besides the conventional therapy, there are several novel pathways and specific targets, on which focus new therapeutics. New therapeutics aim 1./ to correct genetic susceptibility by stimulating NOD2 expression, TLR3 signaling or inhibition of TLR4 pathway, 2./ to restore the immune dysregulation by inhibition of pro-inflammatory cytokines (TNF-, IL-6, IL-13, IL-17, IL-18, IL-21), Th1 polarisation (IL-2, IL-12, IL-23, IFN-), T-cell activation, leukocyte adhesion, as well as by immunostimulation (GM-CSF, G-CSF) and anti-inflammatory cytokines (IL-10, IL-11, IFN--1a), 3./ to restore mucosal barrier function and stimulate mucosal healing by different growth factors, such as GH, EGF, KGF, TGF-, VEGF, 4./ to restore the normal bacterial flora by antibiotics, probiotics. However, in spite of these numerous potential targets, the true value and clinical significance of most of the new biologics and molecules are not clear yet.

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Bifidobacterium lactisattenuates onset of inflammation in a murine model of colitis

Abstract: Daily oral administration of B. lactis was able to reduce inflammatory and T cells mediators and to promote regulatory T cells specific markers in a mouse model of colitis.

Cited by 54 publications

References 62 publications

Host lysozyme-mediated lysis of Lactococcus lactis facilitates delivery of colitis-attenuating superoxide dismutase to inflamed colons

Host lysozyme-mediated lysis of Lactococcus lactis facilitates delivery of colitis-attenuating superoxide dismutase to inflamed colons

Intestinal virome changes precede autoimmunity in type I diabetes-susceptible children

Gut Inflammation: Current Update on Pathophysiology, Molecular Mechanism and Pharmacological Treatment Modalities

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