Seeding the Infant Gut in Early Life—Effects of Maternal and Infant Seeding with Probiotics on Strain Transfer, Microbiota, and Gastrointestinal Symptoms in Healthy Breastfed Infants

We investigated the effects of two dosing regimens of two multi-strain probiotic products on the gut microbiota of breastfed infants, including the transfer of the dosed strains and clinical outcomes. In forty-seven dyads, infants were either exposed through maternal intake (MS) of Lactobacillus acidophilus LA-5, Bifidobacterium animalis subsp. lactis BB-12, Lacticaseibacillus rhamnosus LGG, and Bifidobacterium longum subsp. infantis Bifin02 from gestational week thirty-three until four weeks after birth (n = 24) or dosed directly (IS) with the same strains except for LA-5 starting within 24 h after birth until day 28 (n = 23). Infant stool samples were collected on day 0, 14, 28, and 42 after birth. Gastrointestinal symptoms were assessed by parents using an electronic diary. Microbiota composition was determined using 16S rRNA sequencing, and strain recovery was analyzed by qPCR. Notably, 100% of the IS infants were colonized with Bifin02 after 14 days as opposed to only 25% of the MS infants. Mean stool frequency was significantly lower in IS infants compared to MS infants and IS infants had softer stools on day 14, 28, and 42. A significantly steeper slope of progression of inconsolable crying and fussing was observed in MS infants compared to IS infants. In conclusion, direct infant seeding induced a faster increase in fecal bifidobacteria abundancy and Bifin02 recovery compared to dosed through the maternal intake

In vitro effects of live and heat-inactivated Bifidobacterium animalis subsp. lactis, BB-12 and Lactobacillus rhamnosus GG on Caco-2 cells

Probiotic–host interaction can be cell-to-cell or through metabolite production. Dead (inactive) organisms could interact with the host, leading to local effects and possible health benefits. This research examined the effects of live and heat-inactivated Bifidobacterium animalis subsp. lactis, BB-12 (BB-12) and Lactobacillus rhamnosus GG (LGG) on cultured Caco-2 cells focusing on epithelial integrity and production of inflammatory mediators. Live organisms increased transepithelial electrical resistance (TEER), a barrier-integrity marker, with LGG having a greater effect than BB-12. When mildly heat-treated, both organisms had a more modest effect on TEER than when alive. When they were heat-inactivated, both organisms had only a limited effect on TEER. Neither live nor heat-inactivated organisms affected production of six inflammatory mediators produced by Caco-2 cells compared to control conditions. Pre-treatment with heat-inactivated LGG or BB-12 did not alter the decline in TEER caused by exposure to an inflammatory cocktail of cytokines. However, pre-treatment of Caco-2 cells with heat-inactivated organisms alone or their combination decreased the production of interleukin (IL)-6, IL-18, and vascular endothelial growth factor. To conclude, while the live organisms improve the epithelial barrier using this model, neither live nor heat-inactivated organisms directly elicit an inflammatory response by the epithelium. Pre-treatment with heat-inactivated BB-12 or LGG can reduce some components of the response induced by an inflammatory stimulus

Adipose tissue PCB levels and <i>CYP1B1</i> and <i>COMT</i> genotypes in relation to breast cancer risk in postmenopausal Danish women

<div><p>Exposure to PCBs may be an etiologic factor for breast cancer. The cytochrome P450 1B1 (<i>CYP1B1</i>) and catechol-<i>O</i>-methyltransferase (<i>COMT</i>) enzymes are involved in estrogen metabolism and PCB metabolism, both of which may relate to breast cancer susceptibility. Polymorphisms in genes regulating these enzymes control efficiency. Our objective was to assess whether <i>CYP1B1</i> and <i>COMT</i> gene polymorphisms modulate the effect of PCBs in breast cancer risk, among postmenopausal Danish women. Neither <i>CYP1B1 Leu432Val</i> polymorphisms nor adipose tissue PCBs were independently associated with breast cancer risk. When assessing the independent effect of the <i>COMT Val158Met</i> polymorphism, we observed reduced risk for breast cancer amongst hormone replacement therapy using women who were homozygous carriers of the variant allele compared with those carrying the wild-type variant (RR = 0.41; 95% CI: 0.29–0.89). We found no statistically significant interactions between any of the PCB groups and <i>CYP1B1</i> or <i>COMT</i> polymorphisms on the risk of breast cancer.</p></div