Interaction of orally administered Lactobacillus rhamnosus GG with skin and gut microbiota and humoral immunity in infants with atopic dermatitis

P>Background The intestinal mucosa functions as a defence barrier against gut intraluminar antigens. The maturational events in the gut parallel its step-wise colonization. Atopic dermatitis (AD) is associated with aberrant barrier functions of the skin epithelium and, in a subgroup of patients, of the gut mucosa. Objective To investigate the interaction of Lactobacillus rhamnosus GG (LGG) with skin and gut microbiota and humoral immunity in infants with AD. Methods Thirty-nine infants with AD were randomized for a 3-month period in a double-blind design to receive extensively hydrolysed casein formula supplemented with (n=19) or without (n=20) LGG (ATCC 53103) 5.0 x 107 CFU/g to achieve a daily intake of 3.4 x 109 CFU. Sampling (blood and fecal samples, cotton swab from the skin) was carried out at entry, 1 and 3 months thereafter. Ig-secreting cells were determined by enzyme-linked immunospot and the proportions of CD19+CD27+ B cells among peripheral blood leucocytes by flow cytometry. The major groups of gut and skin bacteria were characterized using PCR. Results The proportions of IgA- and IgM-secreting cells decreased significantly in the treated group; the baseline-adjusted ratios for treated vs. untreated at 1 month were 0.59 (95%CI 0.36-0.99, P=0.044) for IgA- and 0.53 (95%CI 0.29-0.96, P=0.036) for IgM-secreting cells. The proportions of CD19+CD27+ B cells increased in the probiotic-treated infants but not in the untreated. There were no significant differences in bifidobacterial species composition of the gut between the study groups. On the skin, the bacterial counts of Bifidobacterium genus vs. Clostridium coccoides in the treated and untreated infants were similar. Conclusion and Clinical Relevance Specific probiotics may enhance gut barrier function and aid in the development of immune responses. Thus, specific probiotics may afford protection against offending macromolecules in the gut and provide control for future infections by accelerated immunological maturation (ClinicalTrials.gov ID NCT01148667).