Lisa Walters

Maternal obesity during pregnancy is associated with adverse pregnancy outcomes. This might be due to undesired obesity-induced changes in the maternal gut microbiota and related changes in the maternal immune adaptations during pregnancy. The current study examines how obesity affects gut microbiota and immunity in pregnant obese and lean mice during mid-pregnancy (gestational day 12 (GD12)). C57BL/6 mice were fed a high-fat diet or low-fat diet from 8 weeks before mating and during pregnancy. At GD12, we analyzed the gut microbiota composition in the feces and immune responses in the intestine (Peyer’s patches, mesenteric lymph nodes) and the peripheral circulation (spleen and peripheral blood). Maternal obesity reduced beneficial bacteria (e.g., Bifidobacterium and Akkermansia) and changed intestinal and peripheral immune responses (e.g., dendritic cells, Th1/Th2/Th17/Treg axis, monocytes). Numerous correlations were found between obesity-associated bacterial genera and intestinal/peripheral immune anomalies. This study shows that maternal obesity impacts the abundance of specific bacterial gut genera as compared to lean mice and deranges maternal intestinal immune responses that subsequently change peripheral maternal immune responses in mid-pregnancy. Our findings underscore the opportunities for early intervention strategies targeting maternal obesity, ideally starting in the periconceptional period, to mitigate these obesity-related pregnancy effects.

The objective was to assess the effect of peri-implantitis surgery on the peri-implant microbiome with a follow-up of one year. A total of 25 peri-implantitis patients in whom non-surgical treatment has failed to solve peri-implantitis underwent resective surgical treatment. Their peri-implant pockets were sampled prior to surgical treatment (T0) and one year post treatment (T12). The natural dentition was sampled to analyse similarities and differences with the peri-implantitis samples. Treatment success was recorded. The change in microbial relative abundance levels was evaluated. The microbiota was analysed by sequencing the amplified V3-V4 region of the 16S rRNA genes. Sequence data were binned to amplicon sequence variants that were assigned to bacterial genera. Group differences were analysed using principal coordinate analysis, Wilcoxon signed rank tests, and t-tests. Beta diversity analyses reported a significant separation between peri-implantitis and natural dentition samples on T0 and T12, along with significant separations between successfully and non-successfully treated patients. Eubacterium was significantly lower on T12 compared to T0 for the peri-implantitis samples. Treponema and Eubacterium abundance levels were significantly lower in patients with treatment success on T0 and T12 versus no treatment success. Therefore, lower baseline levels of Treponema and Eubacterium seem to be associated with treatment success of peri-implantitis surgery. This study might aid clinicians in determining which peri-implantitis cases might be suitable for treatment and give a prognosis with regard to treatment success.