Bifidobacterium bifidum E3 Combined with Bifidobacterium longum subsp. infantis E4 Improves LPS-Induced Intestinal Injury by Inhibiting the TLR4/NF-κB and MAPK Signaling Pathways In Vivo.

Changes in the functions of the intestinal barrier occur in parallel with the development of sepsis. The protection by Bifidobacterium strains (BB, BL, BB12, and BLBB) was evaluated in mice injected with lipopolysaccharide (LPS). The results revealed an increase in the ratio of ileal villus length to crypt depth in the BLBB group compared with that in the LPS group, as were the number of IgA+ plasma, CD4+/CD8+ T, and dendritic cells. The levels of diamine oxidase (DAO) and d-lactic acid in the serum were lessened in the BLBB group after LPS injection compared with that in the LPS group. In addition, the BLBB group exhibited an increased expression level of tight junction proteins (zonula occludens-1, occludin, and claudin-1), mucin (MUC2) mRNA, reduced NFκB/MAPK signaling pathways, and decreased expression levels of inflammatory cytokines (IL-1ß, IL-6, and TNF-α). The BLBB group enriched the relative abundance of Muribaculaceae, Lachnospiraceae_NK4A136_group, Clostridia_Ucg-014, and Alistipes, resulting in an increase in strains producing short-chain fatty acids. Furthermore, the BLBB group leads to higher levels of deoxycholic acid and biosynthesized linoleate. This study suggested that the BLBB group could enhance the capacity of the intestinal barrier and intestinal mucosal immunity, reduce intestinal inflammation, and improve the composition of gut microbiota. Bifidobacterium bifidum E3 combined with Bifidobacterium longum subsp. infantis E4 may thus serve as a probiotic against the intestinal injury caused by LPS.

Protective effects of tryptophan-catabolizing Lactobacillus plantarum KLDS 1.0386 against dextran sodium sulfate-induced colitis in mice.

Tryptophan is an essential amino acid for the human body, whose intake is through the diet. Several studies support the theory that microbiota-derived tryptophan metabolite played a crucial role in maintaining the balance between gut microbiota and the mucosal immune system. Previously, we selected the Lactobacillus plantarum KLDS 1.0386 strain with high tryptophan-metabolic activity after the screening of 16 Lactobacillus strains. The current study aimed to assess the effects of L. plantarum KLDS 1.0386 combination with tryptophan in improving ulcerative colitis (UC) induced by dextran sodium sulfate (DSS) and the potential mechanisms involved. Our results showed that L. plantarum KLDS 1.0386 combined with tryptophan (LAB + Trp) decreased DAI score, MPO level, and pro-inflammatory cytokine (TNF-α, IL-1ß, and IL-6) concentration. It also increased anti-inflammatory cytokine (IL-10) production, tight junction proteins (claudin-1, occludin, and ZO-1), and mucin (MUC1 and MUC2) mRNA expressions. The level of indole-3-acetic acid (IAA), an important tryptophan metabolite in the liver, serum, and colon, was elevated after LAB + Trp treatment, which further upregulated aryl hydrocarbon receptor (AHR) mRNA expression to activate the IL-22/STAT3 signaling pathway. Moreover, the supplementation with LAB + Trp modulated gut microbiota composition. The present study provided novel insights that can be used to reduce the number of UC patients by employing a method utilizing tryptophan-catabolizing Lactobacillus strains.

In vitro and in vivo evaluation of an exopolysaccharide produced by Lactobacillus helveticus KLDS1.8701 for the alleviative effect on oxidative stress.

Correlations between oxidative stress and degenerative diseases have been gaining increasing attention. A number of studies affirm that exopolysaccharide (EPS) produced by lactic acid bacteria (LAB) can alleviate oxidative stress and further prevent the related diseases. In our previous study, Lactobacillus helveticus KLDS1.8701 has been shown to possess high antioxidant capacity in vitro. The aim of this study was to evaluate the ameliorative effects of EPS produced by L. helveticus KLDS1.8701 on oxidative stress. Firstly, EPS was isolated from the culture of L. helveticus KLDS1.8701 and purified using DEAE-Sepharose Fast Flow chromatography. Secondly, the antioxidant capacities of EPS fractions were evaluated using in vitro methods. Thirdly, an in vivo study was performed to investigate the possible protective effects of EPS on d-galactose (d-gal)-induced liver damage and gut microbiota disorder. In vitro antioxidant activity results suggested that EPS-1 exhibited strong scavenging properties on 2,2-diphenyl-1-picrylhydrazyl radical, superoxide radical, hydroxyl radical, and chelating activity on ferrous ion. In vivo, EPS-1 supplementation significantly attenuated oxidative status such as decreased organic index, liver injury and liver oxidative stress. EPS-1 supplementation shifted the gut microbiota composition to that of the control group. In addition, the analysis of Spearman's rank correlation suggested that the protective effects of EPS correlated with manipulating the gut microbiota composition in d-gal-induced mice. These results implied that EPS-1 supplementation could mitigate hepatic oxidative stress via manipulating the gut microbiota composition and be used as a potential candidate to attenuate oxidative damage.