Abstract
Background and aimsLactulose is a common food ingredient and widely used as a treatment for constipation or hepatic encephalopathy and a substrate for hydrogen breath tests. Lactulose is fermented by the colon microbiota resulting in the production of hydrogen (H2). H2 is a substrate for enteropathogens including Salmonella Typhimurium (S. Typhimurium) and increased H2 production upon lactulose ingestion might favor the growth of H2-consuming enteropathogens. We aimed to analyze effects of single-dose lactulose ingestion on the growth of intrinsic Escherichia coli (E. coli), which can be efficiently quantified by plating and which share most metabolic requirements with S. Typhimurium.Methods32 healthy volunteers (18 females, 14 males) were recruited. Participants were randomized for single-dose ingestion of 50 g lactulose or 50 g sucrose (controls). After ingestion, H2 in expiratory air and symptoms were recorded. Stool samples were acquired at days -1, 1 and 14. We analyzed 16S microbiota composition and abundance and characteristics of E. coli isolates.ResultsLactulose ingestion resulted in diarrhea in 14/17 individuals. In 14/17 individuals, H2-levels in expiratory air increased by ≥20 ppm within 3 hours after lactulose challenge. H2-levels correlated with the number of defecations within 6 hours. E. coli was detectable in feces of all subjects (2 x 102–109 CFU/g). However, the number of E. coli colony forming units (CFU) on selective media did not differ between any time point before or after challenge with sucrose or lactulose. The microbiota composition also remained stable upon lactulose exposure.ConclusionIngestion of a single dose of 50 g lactulose does not significantly alter E. coli density in stool samples of healthy volunteers. 50 g lactulose therefore seems unlikely to sufficiently alter growth conditions in the intestine for a significant predisposition to infection with H2-consuming enteropathogens such as S. Typhimurium (www.clinicaltrials.gov NCT02397512).
Highlights
Humans coexist with trillions of microbes on their body surfaces, collectively referred to as microbiota
E. coli was detectable in feces of all subjects (2 x 102–109 colony forming units (CFU)/g)
The number of E. coli colony forming units (CFU) on selective media did not differ between any time point before or after challenge with
Summary
Humans coexist with trillions of microbes on their body surfaces, collectively referred to as microbiota. One of the key benefits these microbes confer to their host is colonization resistance (CR), i.e. protection against invasion and infection by pathogens. It is conceivable that during gut colonization, the pathogen has to compete with the resident intestinal microbiota for nutrients and binding sites (nutrient-niche hypothesis) [1, 2]. Antibiotic treatment can disturb the intestinal microbiota, predisposing the host to infections with enteric pathogens including Salmonella Typhimurium Likewise, according to the nutrient-niche hypothesis, providing the ecosystem with an additional nutrient should open new niches, which might reduce colonization resistance for certain pathogens. Lactulose is fermented by the colon microbiota resulting in the production of hydrogen (H2). Typhimurium) and increased H2 production upon lactulose ingestion might favor the growth of H2-consuming enteropathogens.
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