Probiotics May Prevent Atopic Dermatitis if Microbiome Cooperates

Previous research showed probiotics given to pregnant women during certain stages of pregnancy and post delivery reduced the likelihood of atopic dermatitis in their children. Recently published reports; however, may not agree.

Scientists had previously reported that probiotics given to pregnant women at term and for three months after delivery reduced the incidence of atopic dermatitis (AD) in their children. But new research now suggests the probiotic may have been a less than protective agent than a factor interacting with an intrinsic gut microbiota unique to the children who did not develop AD.

Knut Rudi, PhD, Department of Chemistry, Biotechnology and Food Science, University of Life Sciences, Ås, Norway and colleagues assessed the Prevention of Allergy among Children in Trondheim (ProPACT) cohort. The team recently reported findings that the probiotic given to the mothers, most of whom had nursed their infants during the three months probiotic regimen, appeared to have "little or no" effect on the gut microbiota composition of children between the time it was characterized 10 days after birth and at two years of age.

Instead, Rudi and colleagues have determined that the children without AD, who appeared to have some protective effect from their mothers receiving probiotic supplementation, actually had a distinctly different microbiota than that of the children who developed AD despite the supplementation.

"Therefore, it is unlikely that the AD effect is through gut microbiota modulation," Rudi and colleagues indicated. "A hypothesis that has not yet been explored, however, is that there are intrinsic differences in the gut microbiota that impact the effect of probiotics on AD."

The new study characterized the gut microbiota of more than 250 mother-child pairs and compared that in children who did and did not develop AD of the mothers on probiotics and the children with and without AD of mothers who did not receive probiotic supplementation.

The children who developed AD despite the probiotic intervention were found to have had an overrepresentation of a bacterium related to Bifidobacterium dentium, compared to children in the other groups. This high representation, six-fold over what would have been expected by chance, remained associated with those who developed AD independent of the mode of delivery or history of atopy in the family.

"Our results support the hypothesis of the probiotic intervention effect being dependent on the intrinsic microbiota, with high levels of B. dentium in combination with a deviating microbiota at 10 days being significantly associated with lack of probiotic intervention effect on AD," Rudi and colleagues declared.

The researchers grappled with the additional quandary that B. dentium could have been expected to be protective rather than contributing to onset of AD, as it produces gamma-aminobutryic acid (GABA) which has immunomodulatory effects associated with reduced levels of AD-like skin lesions in animal models. They speculate that the possible opposite effect found in this study might be attributed to the timing of immunomodulatory processes effecting normal immune development.

Despite the apparent need for future research into the mechanistic roles of B. dentium and GABA in AD development, Rudi and colleagues affirm, "Our results contribute to the importance of early colonization for diseases later in life...(and) point towards the hypothesis that the effect of probiotics in the prevention of AD can be dependent on the intrinsic microbiota."

The study, "Effect of Probiotics in Prevention of Atopic Dermatitis is Dependent on the Intrinsic Microbiota at Early Infancy," was posted on-line December 5 in the Journal of Allergy and Clinical Immunology.

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