The neuroinflammation imaging of bifidobacterium and fecal microbiota
transplantation: therapeutic effects evaluation in chronic hepatic
encephalopathy rats by [18F]PBR146 in-vivo imaging
Abstract
Neuroinflammation plays a significant role in pathogenesis of hepatic
encephalopathy (HE). Radiotracer [18F]PBR146 is used for in-vivo
imaging of neuroinflammation. Bifidobacterium (BIF) and fecal microbiota
transplantation (FMT) are emerging as promising therapeutic approaches
for HE. The objective of this study was to monitor and compare the
treatment efficiencies of BIF and FMT on neuroinflammation in chronic HE
rats [bile duct ligation (BDL) operation] by [18F]PBR146
micro-PET/CT. Thirty rats were divided into Sham+NS, BDL+NS, BDL+BIF,
and BDL+FMT groups. Behavioral assessments, fecal samples collections,
and micro-PET/CT scans were conducted sequentially following the
successful establishment of the chronic HE model. The study analyzed
average %ID/g values of whole brain, brain regions, and main organs
across each group, complemented by biochemical and pathological
analysis. Behavioral results, IL-1β, IL-6, IL-10, and TNF-α levels
showed no significant differences among four groups. Although there was
no significant difference in global brain uptake values of
[18F]PBR146 among four groups (P=0.053), regional brain comparisons
revealed significant discrepancies in bilateral accumbens, retrosplenial
cortex, posterior hippocampus, left striatum, cingulate cortex, right
frontal association cortex, and antero-dorsal hippocampus (all
P<0.05). Sham+NS group was mainly enriched with Parasutterella,
Streptococcus, and Anaeroplasma, the BDL+FMT group with Enterococcus,
Aestuariispira, Lactobacillus, Pseudomonas, and Globicatella, and the
BDL+BIF group with Enterorhabdus. The results suggested that BIF had
inhibitory effect on neuroinflammation in BDL rats, whereas FMT did not
demonstrate positive effects on the chronic HE model rats, might because
of dysbiosis. [18F]PBR146 could effectively and noninvasively
monitor the efficacy of gut-targeted treatment in chronic HE model.