Lactobacillus johnsonii BFE6154 Ameliorates Diet-Induced Hypercholesterolemia

• Published in: Probiotics and antimicrobial proteins Vol. 15; no. 3; pp. 451 - 459
• Main Authors: Yoon, Hongsup, Lee, Yuri, Park, Haryung, Kang, Hye-Ji, Ji, Yosep, Holzapfel, Wilhelm H.
• Format: Journal Article
• Language: English
• Published: New York Springer US 01-06-2023; Springer Nature B.V
• Subjects: Animals; Applied Microbiology; Biomedical and Life Sciences; Caco-2 Cells; Chemistry/Food Science; Cholesterol; Cholesterol, LDL - metabolism; Diet; Epithelial cells; Fermented milk products; Gene expression; High cholesterol diet; High density lipoprotein; High fat diet; Humans; Hypercholesterolemia; Hypercholesterolemia - etiology; Hypercholesterolemia - therapy; Intestine; Lactobacillus johnsonii; Life Sciences; Lipid metabolism; Lipoproteins; Liver X receptors; Low density lipoprotein; Low density lipoprotein receptors; Membrane Transport Proteins - metabolism; Mice; Microbiology; Niemann-Pick disease; Nutrition; Oral administration; Protein Science; Receptor density; Cholesterol uptake; Probiotics; Hypercholesterolemia; Cholesterol efflux; Lactobacillus johnsonii
• ISSN: 1867-1306; 1867-1314
• DOI: 10.1007/s12602-021-09859-4

The functional characteristics of
Lactobacillus johnsonii
BFE6154, first isolated from Maasai traditional fermented milk, were previously identified in vitro, but its cholesterol-lowering properties have not been verified yet. In this study, we investigated the effect of
L. johnsonii
BFE6154 on cholesterol regulation and the mode of action. Stimulation of Caco-2 intestinal epithelial cells with
L. johnsonii
BFE6154 downregulated the gene expression of Niemann-Pick C1-like 1 (NPC1L1) through the activation of liver X receptor (LXR). Also, stimulation of HepG2 cells with the metabolites produced by
L. johnsonii
BFE6154 revealed an increase in the gene expression of low-density lipoprotein receptor (LDLR). Oral administration of
L. johnsonii
BFE6154 in mice receiving a high-fat and high-cholesterol diet (HFHCD), reduced total cholesterol and low-density lipoprotein-cholesterol (LDL) and increased high-density lipoprotein-cholesterol (HDL) in the blood, compared to the control. Diet-induced hypercholesterolemic mice receiving
L. johnsonii
BFE6154 showed a suppression of cholesterol absorption under the control of NPC1L1 in the intestine. Furthermore,
L. johnsonii
BFE6154 consumption ameliorated the hepatic cholesterol level and LDLR expression, which was reduced by HFHCD. These molecular modulations led to the increase of cholesterol excretion and the decrease of cholesterol levels in the feces and liver, respectively. Taken together, these results suggest that
L. johnsonii
BFE6154 may protect against diet-induced hypercholesterolemia through the regulation of cholesterol metabolism in the intestine and liver.