Bifidobacterium longum CCM 7952 Promotes Epithelial Barrier Function and Prevents Acute DSS-Induced Colitis in Strictly Strain-Specific Manner

Abstract

BackgroundReduced microbial diversity has been associated with inflammatory bowel disease (IBD) and probiotic bacteria have been proposed for its prevention and/or treatment. Nevertheless, comparative studies of strains of the same subspecies for specific health benefits are scarce. Here we compared two Bifidobacterium longum ssp. longum strains for their capacity to prevent experimental colitis.MethodsImmunomodulatory properties of nine probiotic bifidobacteria were assessed by stimulation of murine splenocytes. The immune responses to B. longum ssp. longum CCM 7952 (Bl 7952) and CCDM 372 (Bl 372) were further characterized by stimulation of bone marrow-derived dendritic cell, HEK293/TLR2 or HEK293/NOD2 cells. A mouse model of dextran sulphate sodium (DSS)-induced colitis was used to compare their beneficial effects in vivo.ResultsThe nine bifidobacteria exhibited strain-specific abilities to induce cytokine production. Bl 372 induced higher levels of both pro- and anti-inflammatory cytokines in spleen and dendritic cell cultures compared to Bl 7952. Both strains engaged TLR2 and contain ligands for NOD2. In a mouse model of DSS-induced colitis, Bl 7952, but not Bl 372, reduced clinical symptoms and preserved expression of tight junction proteins. Importantly, Bl 7952 improved intestinal barrier function as demonstrated by reduced FITC-dextran levels in serum.ConclusionsWe have shown that Bl 7952, but not Bl 372, protected mice from the development of experimental colitis. Our data suggest that although some immunomodulatory properties might be widespread among the genus Bifidobacterium, others may be rare and characteristic only for a specific strain. Therefore, careful selection might be crucial in providing beneficial outcome in clinical trials with probiotics in IBD.

Fasting-Mimicking Diet Modulates Microbiota and Promotes Intestinal Regeneration to Reduce Inflammatory Bowel Disease Pathology

“…The relative abundance of S24–7 was down by more than two-fold (64.6% to 27.5% ± 7.9%; Table 1) and that of Lactobacillaceae, a family that regulates T cell activity and can reduce the severity of IBD symptoms in experimental models (Damaskos and Kolios, 2008), was increased three-fold (15.5% to 45.2% ± 4.2%; Table 1) in the DSS+FMD compared to DSS group. Bifidobacteriaceae, a microbial family that has been shown to ameliorate symptoms in DSS-colitis models (Srutkova et al, 2015), was found to be uniquely enriched in the DSS+FMD group (0.034% to 2.67% ± 3.56%; Table 1). We also observed a significant increase in the relative abundance of Erysipelotrichaceae (10.5% ± 5.71%; Table 1) in the DSS+FMD group, although the role of this family in the context of IBD is still not clear (Kaakoush, 2015).…”

Probiotics in Gut-Bone Signaling

“…Using other probiotics, such as L. reuteri (R2LC), in IL-10 deficient colitis models attenuated disease development, normalizing gut barrier function and reducing pro-inflammatory cytokines and histological disease score [106]. Consistent with these studies, DSS induced colitis caused increases in gut permeability in female BALB/c mice which was prevented with treatment of Bifidobacterium longum CCM 7952 (Bl) [107]. Additional studies indicate that the modulation of toll-like receptor 9 (TLR9) is necessary for the beneficial effects of probiotics in ulcerative colitis treatment [108].…”

Exploring the role of the microbiota member Bifidobacterium in modulating immune-linked diseases

“…longum 7952, but not B. longum subsp. longum 372, enhanced expression of TJ proteins in the epithelial layer, which was associated with reduced development of DSS-induced symptoms [63]. This was further highlighted by Hsieh et al [57] who also showed that only some species and strains of Bifidobacterium prevented TNF-α-induced disruption of the epithelial barrier, and promoted tight junctions which, in vitro, was attributed to TLR2, but is yet to be defined in vivo.…”