The brown seaweed Alaria esculenta is the second most cultivated species in Europe, and it is therefore of interest to expand its application by developing food products. In this study, a lactic acid bacteria consortium (LAB consortium) consisting of three Lactiplantibacillus plantarum strains (relative abundance ~94%) and a minor amount of a Levilactobacillus brevis strain (relative abundance ~6%) was investigated for its ability to ferment carbohydrates available in brown seaweed. The consortium demonstrated the ability to ferment glucose, mannitol, galactose, mannose, and xylose, of which glucose and mannitol were the most favored substrates. No growth was observed on fucose, mannuronic and guluronic acid. The consortium used different pathways for carbohydrate utilization and produced lactic acid as the main metabolite. In glucose fermentation, only lactic acid was produced, but using mannitol as a carbohydrate source resulted in the co-production of lactic acid, ethanol, and succinate. Xylose fermentation resulted in acetate production. The consortium was also able to utilize laminari-oligosaccharides (DP2-4), obtained after enzymatic hydrolysis of laminarin, and produced lactic acid as a metabolite. The consortium could grow directly on A. esculenta, resulting in a pH decrease to 3.8 after 7 days of fermentation. Incubation of the same seaweed in corresponding conditions without inoculation resulted in spoilage of the seaweed by endogenous bacteria.

Preeclampsia is a severe pregnancy-related inflammatory disease without an effective treatment. The pathophysiology remains partly unknown. However, an increased inflammatory response and oxidative stress are part of the maternal systemic reaction. Recent data have suggested that dysbiosis of the gut microbiome plays a role in preeclampsia as well as other inflammatory diseases. However, dysbiosis in preeclampsia has not been studied in a Scandinavian population. Furthermore, although the fungal flora may also have anti-inflammatory properties, it has never been studied in preeclampsia. We included 25 preeclamptic and 29 healthy third-trimester women for the ITS and 16S sequencing of fungal and bacterial microbiota, respectively. Calprotectin was measured to assess systemic and intestinal inflammatory responses. The fungal diversity differed with BMI and gestational length, suggesting a link between fungi and the immune changes seen in pregnancy. An LEfSe analysis showed 18 significantly differentially abundant bacterial taxa in PE, including enriched Bacteroidetes and depleted Verrucomicrobia and Syntergistota at the phylum level and depleted Akkermansia at the genus level, suggesting a role in the pathophysiology of PE.

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system caused by myelin-specific autoreactive T cells. We previously demonstrated intestinal barrier disruption and signs of inflammation in experimental autoimmune encephalomyelitis (EAE), a model of MS. Fecal calprotectin is a disease activity biomarker in inflammatory bowel diseases, released by neutrophils in response to inflammation. We aimed to further investigate EAE manifestations in the gastrointestinal tract and to determine whether calprotectin is a useful biomarker of intestinal inflammation in EAE. Calprotectin was analyzed in feces, cecal contents, and plasma of EAE mice. Infiltrating neutrophils and goblet cells were investigated in different parts of the gastrointestinal tract before the onset of neurological symptoms and during established disease. We found increased calprotectin levels in feces, cecal content, and plasma preceding EAE onset that further escalated during disease progression. Increased neutrophil infiltration in the intestinal tissue concomitant with IL-17 expression and myeloperoxidase activity was found to correlate well with clinical activity. Increased goblet cells in the intestine, similar to irritable bowel syndrome (IBS), were also observed. The results suggest calprotectin as a good biomarker of gastrointestinal inflammation in EAE and the potential of this model as a useful animal model for IBS.

The brown seaweed Alaria esculenta is the second most cultivated species in Europe and it is therefore of interest to expand its application in developing food products. In this study, a lactic acid bacteria consortium (LAB consortium) consisting of three Lactiplantabacillus plantarum strains (relative abundance ~ 94%) and a minor amount of a Levilactobacillus brevis strain (relative abundance of ~ 6%) was investigated for its ability to ferment carbohydrates available in brown seaweed. The consortium demonstrated ability in fermenting glucose, mannitol, galactose, mannose, and xylose, of which glucose and mannitol were the most favored substrates; no growth was observed on fucose, mannuronic and guluronic acid. The consortium used different pathways for carbohydrate utilization and produced lactic acid as the main metabolite. In glucose fermentations, only lactic acid was produced, but use of mannitol as carbohydrate source, resulted in co-production of lactic acid, ethanol and succinate. Xylose fermentation resulted in acetate production. The consortium was also able to utilize laminari-oligosaccharides (DP 2-4), obtained after enzymatic hydrolysis of laminarin, and produced lactic acid as metabolite. The consortium could grow directly on A. esculenta, resulting in a pH decrease to 3.8 after 7 days of fermentation. Incubation of the same seaweed at corresponding conditions without inoculation resulted in spoilage of the seaweed by endogenous bacteria.

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system caused by myelin-specific autoreactive T cells. We previously demonstrated intestinal barrier disruption and signs of inflammation in experimental autoimmune encephalomyelitis (EAE), a model of MS. Fecal calprotectin is a disease activity biomarker in inflammatory bowel diseases, released by neutrophils in response to inflammation. We aimed to further investigate EAE manifestations in the gastrointestinal tract, and to determine whether calprotectin is a useful biomarker of intestinal inflammation in EAE. Calprotectin was analyzed in feces, cecal contents, and plasma of EAE mice. Infiltrating neutrophils and goblet cells were investigated in different parts of the gastrointestinal tract, before onset of neurological symptoms and during established disease. We found increased calprotectin levels in feces, cecal content and plasma, preceding EAE onset that further escalated during disease progression. Increased neutrophil infiltration in the intestinal tissue concomitant with IL-17 expression and myeloperoxidase activity was found correlating well with clinical activity. Increased goblet cells in intestine similar to irritable bowel syndrome (IBS) were also observed. The results suggest calprotectin as a good biomarker of gastrointestinal inflammation in EAE, also the potential of this model as a useful animal model for IBS.