Dietary fructo-oligosaccharides and lactulose inhibit intestinal colonisation but stimulate translocation of salmonella in rats.
OBJECTIVE
It is frequently assumed that dietary non-digestible carbohydrates improve host resistance to intestinal infections by stimulating the protective gut microflora. However, compelling scientific evidence from in vivo infection studies is lacking. Therefore, we studied the effect of several non-digestible carbohydrates on the resistance of rats to Salmonella enteritidis infection.


METHODS
Rats (n=8 per group) were fed "humanised" purified diets containing 4% lactulose, fructo-oligosaccharides (FOS), resistant starch, wheat fibre, or cellulose. After an adaptation period of 2 weeks the animals were orally infected with S enteritidis. Supplement induced changes in faecal biochemical and microbiological parameters were studied before infection. Colonisation of salmonella was determined by studying the faecal excretion of this pathogen and translocation by analysis of urinary nitric oxide metabolites over time and classical organ cultures. Intestinal mucosal myeloperoxidase activity was determined to quantify intestinal inflammation after infection.


RESULTS
Despite stimulation of intestinal lactobacilli and bifidobacteria and inhibition of salmonella colonisation, FOS and lactulose significantly enhanced translocation of this pathogen. These supplements also increased cytotoxicity of faecal water and faecal mucin excretion, which may reflect mucosal irritation. In addition, caecal and colonic, but not ileal, mucosal myeloperoxidase activity was increased in infected rats fed FOS and lactulose. In contrast, cellulose, wheat fibre, and resistant starch did not affect the resistance to salmonella.


CONCLUSIONS
In contrast to most expectations, FOS and lactulose impair the resistance of rats to intestinal salmonella infection. Obviously, stimulation of the endogenous lactobacilli and bifidobacteria is no guarantee of improved host defence against intestinal infections.
Bovee-Oudenhoven
I M J
IM
Wageningen Centre for Food Sciences, Ede, The Netherlands. Ingeborg.Bovee@nizo.nl
ten Bruggencate
S J M
SJ
Lettink-Wissink
M L G
ML
van der Meer
R
R
D000284:Administration, Oral; D000818:Animals; D018988:Bacterial Translocation / Q000187:drug effects* / Q000502:physiology; D002482:Cellulose / Q000008:administration & dosage; D004040:Dietary Carbohydrates / Q000008:administration & dosage*; D004043:Dietary Fiber / Q000008:administration & dosage; D004751:Enteritis / Q000382:microbiology; D005243:Feces / Q000382:microbiology; D007410:Intestinal Diseases / Q000382:microbiology; D007413:Intestinal Mucosa / Q000382:microbiology; D007422:Intestines / Q000201:enzymology / Q000382:microbiology; D007792:Lactulose / Q000008:administration & dosage*; D008297:Male; D009077:Mucins / Q000378:metabolism; D009844:Oligosaccharides / Q000008:administration & dosage*; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012481:Salmonella Infections, Animal / Q000382:microbiology*; D012477:Salmonella enteritidis / Q000502:physiology*; D013047:Specific Pathogen-Free Organisms; D013213:Starch / Q000008:administration & dosage; D014908:Triticum
D004040:Dietary Carbohydrates; D004043:Dietary Fiber; D009077:Mucins; D009844:Oligosaccharides; D007792:Lactulose; D002482:Cellulose; D013213:Starch; D009195:Peroxidase