Simultaneous Amelioratation of Colitis and Liver Injury in Mice by Bifidobacterium longum LC67 and Lactobacillus plantarum LC27.
Se-Eun JangJin-Ju JeongJeon-Kyung KimMyung Joo HanDong-Hyun KimPublished in: Scientific reports (2018)
Disturbances in the gut microbiota composition are associated with chronic inflammatory diseases of the intestine and the liver. In a preliminary study, Lactobacillus plantarum LC27 and Bifidobacterium longum LC67 could inhibit Escherichia coli growth and lipopolysaccharide-induced NF-κB activation linked to gut inflammation. Here, we investigated their effects on 2,4,6-trinitrobenzesulfonic acid (TNBS)-induced colitis and liver damage in mice. First, oral administration of LC27 or LC67 (1 × 109 CFU/mouse) inhibited TNBS-induced colon shortening [F(5,30) = 100.66, P < 0.05] and myeloperoxidase activity [F(5,30) = 56.48, P < 0.05]. These probiotics restored TNBS-induced disturbance of gut microbiota, leading to the suppression of Proteobacteria to Bacteroidetes ratio and fecal and blood lipopolysaccharide levels. Second, LC27 and LC67 inhibited TNBS-induced NF-κB activation, reversed TNBS-suppressed tight junction protein expression, and restored Th17/Treg balance. Also, treatment with LC27 or LC67 significantly decreased TNBS-induced alanine transaminase [ALT, F(5,30) = 3.50, P < 0.05] and aspartate transaminase [AST, F(5,30) = 12.81, P < 0.05] levels in the blood, as well as t-butylhydroperoxide-induced ALT and AST levels. Finally, the mixture of LC27 and LC67 (0.5 × 109 CFU/mouse, respectively) synergistically attenuated TNBS- or t-butylhydroperoxide-induced colitis and liver damage. The capability of LC27 and LC67 to reverse TNBS-mediated microbiota shift and damage signals suggests that these probiotics may synergistically attenuate colitis and liver injury by alleviating gut microbiota imbalance.
Keyphrases
- simultaneous determination
- drug induced
- liver injury
- oxidative stress
- mass spectrometry
- escherichia coli
- liquid chromatography
- high glucose
- lipopolysaccharide induced
- toll like receptor
- type diabetes
- tandem mass spectrometry
- lps induced
- adipose tissue
- immune response
- endothelial cells
- pseudomonas aeruginosa
- nuclear factor
- cell proliferation
- single molecule
- insulin resistance
- replacement therapy