Fructo-oligosaccharides and skin inflammation

Abstract

The indigenous gut microbiota present early in life is thought to play an important role in the pathogenesis of allergic diseases including atopic dermatitis, and strategies to manipulate the gut microbiota in infancy have been considered in preventing the development of such diseases. Gut microbiota in breast-fed infants is dominated by bifidobacteria, and breast milk is protective against atopic dermatitis. Considering that fermentation of breast milk oligosaccharides in the gut results in the proliferation of bifidobacteria, supplementation of non-digestible oligosaccharides, such as fructo-oligosaccharides, to infant formula could increase bifidobacteria in the gut, which may in turn protect against atopic dermatitis. Indeed, recent human interventions have demonstrated that supplementation of oligosaccharide mixtures containing high-molecular mass fructo-oligosaccharides to infant formula reduced the incidence of atopic dermatitis. In addition, supplementation of kestose, a low-molecular mass fructo-oligosaccharide, reportedly reduced the disease severity in infants with atopic dermatitis. These human studies suggest that fructo-oligosaccharides exert preventive and therapeutic effects on atopic dermatitis in infants. Animal studies have also shown that fructo-oligosaccharide supplementation reduced the severity of atopic dermatitis-like skin inflammation and allergic contact dermatitis. Although the mechanism by which fructo-oligosaccharides affect the development of atopic dermatitis remains to be elucidated, the development of animal models would enable mechanistic studies. Previous animal studies showed that dietary fructo-oligosaccharides increased production of secretory immunoglobulin A and interleukin-10 in the gut, which may be advantageous in the prevention of food allergy. One possible mechanism by which fructo-oligosaccharides modulate the immune response is linked to gut microbiota. Recognition of microbe-associated molecular patterns and short-chain fatty acids (i.e. fermentation products of non-digestible oligosaccharides in the gut) by specific receptors in the gut may modulate immune responses. Another possible mechanism is that fructo-oligosaccharides may be absorbed intact in the gut and interact directly with immune cells outside the intestinal tract. Because the clinical data are currently insufficient to recommend prebiotics as part of a standard protocol in the prevention and treatment of atopic dermatitis, additional well-designed prospective clinical trials and mechanistic studies using appropriate animal models are needed to advance knowledge in this field.