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Preeclampsia is a leading cause of morbidity and mortality in pregnant women, affecting 5–8% of gestations worldwide. Its development is influenced by maternal immune abnormalities, metabolic disorders, and gut dysbiosis. In this study, we show that gut dysbiosis in pregnant C57BL/6J dams leads to increased fetal resorption, impaired placental development and altered vascularization. These adverse outcomes are associated with key pathological features of preeclampsia, including hypoxia, endoplasmic reticulum (ER) stress and reduction in uterine natural killer (NK) cell numbers. Furthermore, gut dysbiosis significantly perturbs placental carbohydrate metabolism, which impairs NK cell IFN-γ secretion. Notably, glucose supplementation restores placental NK cell function and reduces fetal resorption, suggesting that the observed impairment is reversible and dependent on a lower glycolytic rate. These findings highlight maternal gut microbiota as a key player in carbohydrate metabolism, with a pivotal role in modulating placental immunity and pregnancy outcome. The results provide valuable insights into potential metabolic biomarkers and suggest that targeting the gut microbiota may offer a strategy for preventing preeclampsia. Preeclampsia is a leading cause of morbidity and mortality in pregnancy and has multiple causes. Here the authors examine how changes in the gut microbiota alter pregnancy outcome and show changes in fetal reabsorption along with reduction in placental NK cell IFN-γ production accompanied by perturbation of placental carbohydrate metabolism.

Skin inflammation and damage of skin barrier integrity contribute to the pathogenesis of inflammatory skin diseases such as psoriasis and atopic dermatitis. Nowadays, there is a growing interest in alternative and complementary strategies to counteract skin inflammation and treat dermatologic conditions. Postbiotics, metabolites released during bacterial fermentation, exert anti-inflammatory proprieties and contribute to the maintenance of epithelial barrier integrity. Therefore, we investigated the effect of LP-PBL, a novel Lactobacillus paracasei CNCM I-5220-derived postbiotic, in controlling skin inflammation and protecting the skin barrier. We performed RNA-sequencing on Poly(I:C)-stimulated keratinocytes and investigated LP-PBL efficacy in regulating pro-inflammatory cytokine release. The production of most relevant cytokines was demonstrated by ELISA. Then, we tested postbiotic lenitive efficacy on healthy volunteers’ irritated skin. We compared the effect of a postbiotic-containing cream formulation versus placebo on sodium lauryl sulphate treated skin. We demonstrate that LP-PBL has anti-inflammatory activity by modulating Poly(I:C)-dependent inflammatory pathways and pro-inflammatory cytokine release in keratinocytes. The postbiotic inhibited the upregulation of interleukin (IL)-23A, which is overexpressed in psoriatic skin, and of IL-33 and thymic stromal lymphopoietin (TSLP) that are upregulated in atopic dermatitis. Moreover, it increased filaggrin and zonula occludens (ZO)-1 expression in Poly(I:C)-stimulated keratinocytes, suggesting beneficial effects on inflamed and damaged skin. Consistently, a clinical test on healthy volunteers showed that topic LP-PBL treatment significantly reduced skin redness upon sodium lauryl sulphate challenge compared to placebo, leading to a rapid recovery of the irritated skin. Overall, we demonstrated the protective role of LP-PBL on the skin, both in vitro and in the clinical test, suggesting that postbiotic topical application could represent an innovative and promising strategy to counteract skin inflammation and preserve skin barrier integrity.