Abstract
Non-caloric artificial sweeteners are frequently discussed as components of the “Western diet”, negatively modulating intestinal homeostasis. Since the artificial sweetener saccharin is known to depict bacteriostatic and microbiome-modulating properties, we hypothesized oral saccharin intake to influence intestinal inflammation and aimed at delineating its effect on acute and chronic colitis activity in mice. In vitro, different bacterial strains were grown in the presence or absence of saccharin. Mice were supplemented with saccharin before or after induction of acute or chronic colitis using dextran sodium sulfate (DSS) and the extent of colitis was assessed. Ex vivo, intestinal inflammation, fecal bacterial load and composition were studied by immunohistochemistry analyses, quantitative PCR, 16 S RNA PCR or next generation sequencing in samples collected from analyzed mice. In vitro, saccharin inhibited bacterial growth in a species-dependent manner. In vivo, oral saccharin intake reduced fecal bacterial load and altered microbiome composition, while the intestinal barrier was not obviously affected. Of note, DSS-induced colitis activity was significantly improved in mice after therapeutic or prophylactic treatment with saccharin. Together, this study demonstrates that oral saccharin intake decreases intestinal bacteria count and hence encompasses the capacity to reduce acute and chronic colitis activity in mice.
Highlights
Inflammatory bowel disease (IBD) with its two main subentities, Crohn’s disease (CD) and ulcerative colitis (UC), comprises a group of chronic, relapsing-remitting, immune-mediatedNutrients 2020, 12, 1122; doi:10.3390/nu12041122 www.mdpi.com/journal/nutrientsNutrients 2020, 12, 1122 inflammatory disorders of the human gastrointestinal tract
Alterations in intestinal bacterial composition is often observed in IBD and intestinal bacterial overgrowth confers the risk of intestinal inflammation [5,37]
We first studied the direct effect of saccharin on bacterial growth from exemplary bacterial species, with 5 mM saccharin exhibiting bacteriostatic but not bactericidal effects on Staphylococcus aureus (Firmicute), Klebsiella pneumonia and Pseudomonas aeruginosa (Figure 1a,b)
Summary
Inflammatory bowel disease (IBD) with its two main subentities, Crohn’s disease (CD) and ulcerative colitis (UC), comprises a group of chronic, relapsing-remitting, immune-mediatedNutrients 2020, 12, 1122; doi:10.3390/nu12041122 www.mdpi.com/journal/nutrientsNutrients 2020, 12, 1122 inflammatory disorders of the human gastrointestinal tract. One group of nutritional compounds which has been discussed to confer to the risk of UC is non-caloric artificial sweeteners (NAS) in general and saccharin (C7 H5 NO3 S) [6]. These synthetic compounds are hundreds of times sweeter than the table sugar sucrose with saccharin itself having a sweetness 200–700 times of table sugar [7]. Absorption differs between animal species depending on the stomach pH, with increased absorption found in species with a lower stomach pH, such as humans, compared with species with a higher stomach pH, including rats and mice [12] This phenomenon will most likely result in a higher proportion of saccharin reaching the gastrointestinal tract in rodents compared to humans
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