Consumption of indigestible saccharides and administration of Bifidobacterium pseudolongum reduce mucosal serotonin in murine colonic mucosa

Abstract

Short-chain fatty acids (SCFAs) increase serotonin (5-hydroxytryptamine, 5-HT) synthesis and content in the colon in vitro and ex vivo, but little is known in vivo. We tested whether dietary indigestible saccharides, utilized as a substrate to produce SCFAs by gut microbiota, would increase colonic 5-HT content in mice. Male C57BL/6J mice were fed a purified diet and water supplemented with 4% (w/v) 1-kestose (KES) for 2 weeks. Colonic 5-HT content and enterochromaffin (EC) cell numbers were lower in mice supplemented with KES than those without supplementation, while monoamine oxidase A activity and mRNA levels of Tph1, Chga, Slc6a4 and Maoa genes in the colonic mucosa, serum 5-HT concentration and total 5-HT content in the colonic contents did not differ between groups. Cecal acetate concentration and Bifidobacterium pseudolongum population were higher in KES-supplemented mice. Similar trends were observed in mice supplemented with other indigestible saccharides, i.e., fructooligosaccharides, inulin and raffinose. Intragastric administration of live B. pseudolongum (108 colony-forming units/day) for 2 weeks reduced colonic 5-HT content and EC cell numbers. These results suggest that changes in synthesis, reuptake, catabolism and overflow of 5-HT in the colonic mucosa are not involved in the reduction of colonic 5-HT content by dietary indigestible saccharides in mice. We propose that gut microbes including B. pseudolongum could contribute to the reduction of 5-HT content in the colonic mucosa via diminishing EC cells.

Enteric Microbiota-Mediated Serotonergic Signaling in Pathogenesis of Irritable Bowel Syndrome

“…Clostridium ramosum stimulates host 5-HT secretion and programs the differentiation of colonic intestinal stem progenitors toward a secretory 5-HT-producing lineage [87]. In contrast, Bifidobacterium pseudolongum reduces the content of 5-HT in colonic mucosa by reducing EC cells [103]. These observations indicate that EC cells are regulated by specific bacteria and induction of aberrant serotonergic signaling by dysbiosis.…”

Dendrobium officinale Endophytes May Colonize the Intestinal Tract and Regulate Gut Microbiota in Mice

“…DO28 increased the relative abundance of fungal genera, including Pyxidiophora , Cladosporium , Talaromyces , Rhodotorula , Filobasidium , and decreased Aspergillus , Mortierella , Penicillium , Cutaneotrichosporon , Candida , compared with those in C28 and ASDO28 groups ( Figure 3(b) ). Our results also indicated that DO28 altered the gut microbiota structure in mice by increasing the beneficial bacteria Lactobacillus murinus [ 37 ], Lactobacillus johnsonii [ 38 ], Bifidobacterium pseudolongum [ 39 ], and Lactobacillus reuteri [ 40 ], and reducing harmful bacteria Ochrobactrum anthropi [ 41 ], Aerococcus urinaeequi [ 42 ], and Clostridium sp. cTPY-12 [ 43 ], compared with those in C28 and ASDO28 groups (Supplement Figure 4(a) ).…”

“…To know which are the primary butyrate-producing bacteria, the synthase that is responsible for butyrate synthesis should be investigated. This study indicated that DO cause an increase in the relative abundance of some SCFAs-producing bacteria Lactobacillus johnsonii [ 38 ], Bifidobacterium pseudolongum [ 39 ], and Lactobacillus reuteri [ 40 ], and decreased some pathobionts Ochrobactrum anthropi [ 41 ], Aerococcus urinaeequi [ 42 ], Clostridium sp. cTPY-12 [ 43 ].…”

Dendrobium officinale Endophytes May Colonize the Intestinal Tract and Regulate Gut Microbiota in Mice

“…DO28 increased the relative abundance of fungal genera, including Pyxidiophora, Cladosporium, Talaromyces, Rhodotorula, Filobasidium, and decreased Aspergillus, Mortierella, Penicillium, Cutaneotrichosporon, Candida, compared with those in C28 and ASDO28 groups (Figure 3(b)). Our results also indicated that DO28 altered the gut microbiota structure in mice by increasing the beneficial bacteria Lactobacillus murinus [37], Lactobacillus johnsonii [38], Bifidobacterium pseudolongum [39], and Lactobacillus reuteri [40], and reducing harmful bacteria Ochrobactrum anthropi [41], Aerococcus urinaeequi [42], and Clostridium sp. cTPY-12 [43], compared with those in C28 and ASDO28 groups (Supplement Figure 4(a)).…”

“…is study indicated that DO cause an increase in the relative abundance of some SCFAs-producing bacteria Lactobacillus johnsonii [38], Bifidobacterium pseudolongum [39], and Lactobacillus reuteri [40], and decreased some pathobionts Ochrobactrum anthropi [41], Aerococcus urinaeequi [42], Clostridium sp. cTPY-12 [43].…”