The gut of preterm neonates is colonised with a paucity of bacterial species originating more from the environment than from the mother. Furthermore, a delayed colonisation by bifidobacteria promotes colonisation by potentially pathogenic bacteria. This may contribute towards the development of neonatal necrotising
enterocolitis (NEC). The physiopathology of NEC is still unclear but immaturity of the gut,
enteral feeding and bacterial colonisation are all thought to be involved. None of the current preventive treatments are considered satisfactory. Modulating the autochthonous microflora by probiotics or
prebiotics could be a more reliable approach to prevention. Using gnotobiotic quails as an experimental model of NEC we have shown that onset of intestinal lesions requires a combination of low endogenous
lactase activity,
lactose in diet, and colonisation by
lactose-fermenting bacteria such as the clostridia. The protective role of bifidobacteria was demonstrated in this model through a decrease in clostridial populations and in
butyric acid.
Oligofructose dietary supplementation was shown to enhance this effect with an increase in the bifidobacterial level and consequently a greater decrease in clostridia. However,
oligofructose was unable to promote a bifidobacterial acquisition when the microflora was initially deprived of this group. Nevertheless,
oligofructose can act as an
anti-infective agent and decrease the occurrence or severity of the lesions depending on the bacteria involved. According to these results and to the fact that
oligosaccharides are a major component of breast milk, the addition of
oligofructose in formula milks may be a nutritional approach to favouring colonisation by a beneficial flora.