Abstract
The gut microbiome is closely related to gut metabolic functions, and the gut microbiome and host metabolic functions affect each other. Clostridium butyricum MIYAIRI 588 (CBM 588) upregulates protectin D1 production in host colon tissue following G protein-coupled receptor (GPR) 120 activation to protect gut epithelial cells under antibiotic-induced dysbiosis. However, how CBM 588 enhances polyunsaturated fatty acid (PUFA) metabolites remains unclear. Therefore, we focused on the metabolic function alterations of the gut microbiome after CBM 588 and protectin D1 administration to reveal the interaction between the host and gut microbiome through lipid metabolism during antibiotic-induced dysbiosis. Consequently, CBM 588 modified gut microbiome and increased the butyric acid and oleic acid content. These lipid metabolic modifications induced GPR activation, which is a trigger of ERK 1/2 signaling and directed differentiation of downstream immune cells in the host colon tissue. Moreover, endogenous protectin D1 modified the gut microbiome, similar to CBM 588. This is the first study to report that CBM 588 influences the interrelationship between colon tissue and the gut microbiome through lipid metabolism. These findings provide insights into the mechanisms of prevention and recovery from inflammation and the improvement of host metabolism by CBM 588.
Highlights
The gut microbiome contributes to the maintenance of homeostasis in host metabolism [1,2].When the gut microbiome is disturbed, metabolites fluctuate significantly [3]
To compare the results of gut microbiome data, we determined α-diversity with Chao1 index (Figure 1C) and found that the mean Chao1 index was significantly lower in the groups that were administered CLDM only, Clostridium butyricum MIYAIRI 588 (CBM 588) + CLDM combination, and protectin D1 + CLDM combination groups than in the control group (p = 0.009, respectively)
Set at p < 0.05. * p < 0.05, compared with control. This trans-omics analysis of the gut microbiome and long-chain fatty acid metabolome in mouse feces was performed to determine the effect of gut microbiota on host lipid metabolism and host-produced metabolites on the gut microbiota
Summary
The gut microbiome contributes to the maintenance of homeostasis in host metabolism [1,2]. When the gut microbiome is disturbed, metabolites fluctuate significantly [3]. Disturbance of this complex system is associated with diseases such as inflammatory bowel diseases (IBDs), which present with chronic persistent inflammation of the digestive tract [4,5]. Gastrointestinal mucosa-related diseases and insulin resistance, obesity, and non-alcoholic fatty liver disease (NASH) have revealed that gut dysbiosis is one of the causes of abnormal host metabolism due to a decrease in beneficial bacteria [6,7,8]. To develop a treatment method for dysbiosis-induced gut
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