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Page 10 of 14 Chen et al. Microbiome Res Rep 2025;4:6 https://dx.doi.org/10.20517/mrr.2024.38

Figure 7. The effect of L. johnsonii CCFM1376 on the FXR signaling pathway in hypercholesterolemic mice. (A) FXR in the ileum; (B)
FGF15; (C) FXR in the liver; (D) SHP; (E) CYP7A1. Different letters in each group indicated significant differences (P < 0.05). FXR:
Farnesoid X receptor; FGF15: fibroblast growth factor 15; SHP: small heterodimer partner.

A previous study has structurally identified a predictive circuit capable of discerning BSH preferences for
glycine or taurine substrates through the detection of BSH diversity among intestinal Lactobacillaceae and
other symbiotic bacteria . Utilizing this circuit, a strain of L. johnsonii with three BSH genes was
[13]
discovered, where two genes demonstrated a preference for glycine, while one gene exhibited a preference
for taurine. L. johnsonii CCFM1376 has demonstrated a preference for glycine-conjugated bile acids. Under
identical conditions, L. johnsonii BFE1061 exhibited a BSH activity of 0.2231 μmol·min ·mL toward
-1
-1
glycodeoxycholic acid . L. johnsonii BFE1061 has also been demonstrated to possess the ability to alleviate
[20]
hypercholesterolemia in mice .
[21]
In this study, mice fed a high-cholesterol diet exhibited altered blood lipid levels. Compared to the control
group, the model group mice showed a notable rise in serum levels of TC and LDL-C. Supplementation
with L. johnsonii CCFM1376 led to an improvement in blood lipid profiles, with significant reductions in
serum TC and LDL-C levels, and a notable rise in HDL-C levels. Similarly, L. johnsonii BFE6154
significantly lowered the serum TC and LDL-C levels and markedly increased the serum HDL-C levels in
[21]
hypercholesterolemic mice . L. johnsonii N6.2 significantly reduced the serum TC levels in mice with diet-
induced obesity . The serum TG levels in mice on a high-cholesterol diet in this study did not show
[22]
significant changes, which may be due to the type of diet fed, a finding that has also been confirmed in other
studies utilizing the same dietary components .
[14]
The liver is the primary site for cholesterol synthesis and metabolism in the human body. When the intake
of cholesterol exceeds the body’s needs and the liver’s capacity to process it, cholesterol may accumulate in