Postbiotic Potential of Heat-Killed Lacticaseibacillus paracasei HP7 in Functional Dyspepsia
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Functional dyspepsia (FD) is a complex gastrointestinal disorder involving impaired motility and digestive dysfunction. This study investigated the postbiotic potential of heat-killed Lacticaseibacillus paracasei HP7 (HP7) in a loperamide-induced FD mouse model. Oral administration of heat-killed HP7 improved gastric emptying, and upregulated expression of genes related to smooth muscle contraction. Heat-killed HP7 treatment also modulated key gastrointestinal hormones, including gastrin (GAS), glucose-dependent insulinotropic peptide (GIP), and peptide YY (PYY), and restored the activities of digestive enzymes such as amylase and trypsin. To investigate potential mechanisms, heat-killed HP7 and exopolysaccharides (EPS) and surface-layer proteins (SLPs) derived from HP7 were applied to LPS-treated Caco-2 cells. These functional components strengthened epithelial barrier function by upregulating tight junction-related genes and reducing the expression of inflammatory genes. These results suggest that heat-killed HP7 and its functional cell surface molecules promoted gastric motility, strengthened barrier integrity, and mitigated inflammation through complementary pathways, indicating their potential as safe and effective postbiotic interventions for managing FD.
Abstract
Functional dyspepsia (FD) is a complex gastrointestinal disorder involving impaired motility and digestive dysfunction. This study investigated the postbiotic potential of heat-killed Lacticaseibacillus paracasei HP7 (HP7) in a loperamide-induced FD mouse model. Oral administration of heat-killed HP7 improved gastric emptying, and upregulated expression of genes related to smooth muscle contraction. Heat-killed HP7 treatment also modulated key gastrointestinal hormones, including gastrin (GAS), glucose-dependent insulinotropic peptide (GIP), and peptide YY (PYY), and restored the activities of digestive enzymes such as amylase and trypsin. To investigate potential mechanisms, heat-killed HP7 and exopolysaccharides (EPS) and surface-layer proteins (SLPs) derived from HP7 were applied to LPS-treated Caco-2 cells. These functional components strengthened epithelial barrier function by upregulating tight junction-related genes and reducing the expression of inflammatory genes. These results suggest that heat-killed HP7 and its functional cell surface molecules promoted gastric motility, strengthened barrier integrity, and mitigated inflammation through complementary pathways, indicating their potential as safe and effective postbiotic interventions for managing FD.Functional dyspepsia (FD) is a complex gastrointestinal disorder involving impaired motility and digestive dysfunction. This study investigated the postbiotic potential of heat-killed Lacticaseibacillus paracasei HP7 (HP7) in a loperamide-induced FD mouse model. Oral administration of heat-killed HP7 improved gastric emptying, and upregulated expression of genes related to smooth muscle contraction. Heat-killed HP7 treatment also modulated key gastrointestinal hormones, including gastrin (GAS), glucose-dependent insulinotropic peptide (GIP), and peptide YY (PYY), and restored the activities of digestive enzymes such as amylase and trypsin. To investigate potential mechanisms, heat-killed HP7 and exopolysaccharides (EPS) and surface-layer proteins (SLPs) derived from HP7 were applied to LPS-treated Caco-2 cells. These functional components strengthened epithelial barrier function by upregulating tight junction-related genes and reducing the expression of inflammatory genes. These results suggest that heat-killed HP7 and its functional cell surface molecules promoted gastric motility, strengthened barrier integrity, and mitigated inflammation through complementary pathways, indicating their potential as safe and effective postbiotic interventions for managing FD.