Aims Atopic disorders are common in young children. The development of atopy may be influenced by exposure to microbes in early life. We tested the hypothesis that administration of a multi-strain probiotic during pregnancy and to young infants would prevent atopy in childhood. Methods Pregnant women from 36 weeks gestation and their infants to age 6 months took daily either a probiotic consisting of two strains of lactobacilli and two strains of bifidobacteria or a matching placebo. Most infants had a first degree relative with atopy. The primary outcome was diagnosed eczema at age 2 years. Secondary outcomes were skin prick responses (SPRs) to common allergens and immune responses measured at birth and age 6 months. Results 220 infants were randomised to the probiotic and 234 to the placebo group. A similar proportion of infants in the probiotic and placebo group developed eczema (34.1% and 32.4% respectively; p=0.71). A SPR to one or more common allergens occurred in 18/171 (10.5%) infants in the probiotic and 32/173 (18.5%) in the placebo group (OR 0.52, 95% CI 0.28-0.98). The main difference between the groups was in early sensitisation to cow's milk and hen's egg proteins. Atopic eczema (eczema and a positive SPR) occurred in 9/171 (5.3%) children in the probiotic and 21/173 (12.1%) in the placebo group (OR 0.40, 95% CI 0.18-0.91). Cord blood eosinophil count was reduced (p=0.024) and stimulated IL-12p70 concentrations in venous blood at age 6 months elevated (p = 0.022) in the probiotic compared with the control group. Conclusions The probiotic reduced the frequency of atopic eczema and atopic sensitisation and promoted a Th1 orientation of the immune system. Probiotics administered during pregnancy and early infancy may be effective in the prevention of atopy.
Objective: The objective of this study was to identify the immunomodulatory potential of two consortia of lactic acid bacteria, "Lab4" and "Lab4b", using human macrophages as an in vitro model system. Methods: THP-1 monocyte-derived macrophages were exposed to metabolites of Lab4 or Lab4b. RT-qPCR was performed on macrophages to determine the expression of M1 pro-inflammatory (IL-1β, IL-18 and CD80) or M2 antiinflammatory (CD206) marker mRNA in addition to IL-1β protein and inflammasome (NLRP3, Caspase-1, NLRP1, NLRC4 and AIM2) mRNA expression. Bacterial (LPS and ATP) and viral (Poly I:C) challenge were simulated to determine the potential of these consortia to regulate IL-1β protein, inflammasome mRNA expression, and antiviral IL-12 mRNA expression and protein under inflammatory conditions. The ability of these consortia to modulate macrophage phagocytosis of E. coli was also assessed. Results: Lab4 and Lab4b metabolites promoted an M1 phenotype in macrophages in vitro by increasing mRNA expression of IL-1β, IL-18, and CD80 and reducing mRNA expression of CD206. Induction of IL-1β protein suggested involvement of the inflammasome. mRNA expression of NLRP3, Caspase-1, NLRP1 and AIM2 was induced by Lab4 and mRNA expression of NLRP3 and Caspase-1 was induced by Lab4b suggesting different potential modes of action of the two consortia. Lab4 and Lab4b metabolites, in combination with this LPS and ATP challenge, enhanced IL-1β mRNA and protein expression further, accompanied by different mRNA expression profiles of inflammasome genes by the two consortia. Lab4 and Lab4b also induced expression of mRNA and protein of the antiviral response gene, IL-12. In combination with Poly I:C challenge, Lab4 induced IL-12 protein further, while Lab4b induced IL-12p25/IL-12p40 mRNA further highlighting potential differences. Both consortia were also able to induce phagocytosis of E. coli particles. Conclusion: Data generated from this study suggest the potential for organism-dependent control of the immunoregulatory response seen in human macrophages.
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