Immune regulation by activation markers at feto-maternal interface in infection-associated spontaneous preterm birth

The role of the placenta-brain axis in psychoneuroimmune programming

“…Our work and others’ point to a role for placental IL-17 and upstream IL-6 mechanisms in PNI programming. Placental diseases ranging from preeclampsia ( Lu et al, 2020 ; Eghbal-Fard et al, 2019 ; Molvarec et al, 2015 ; Pinheiro et al, 2013 ; Sowmya et al, 2015 ; Cornelius et al, 2016 ; Lockwood et al, 2008 ; Radulescu et al, 2016 ) to infection-associated spontaneous preterm birth ( Bhati et al, 2023 ), placental insufficiency ( Darmochwal-Kolarz et al, 2017 ), chorioamnionitis ( Lawrence et al, 2018 ), and chronic stress ( Bronson et al, 2014 ; Diz-Chaves et al, 2012 ; Gumusoglu et al, 2017 ; Mouihate et al, 2016 ; Veru et al, 2015 ) feature increased maternal-placental IL-17 and -6 and have a pathoetiology that is dependent on these cytokines ( Eghbal-Fard et al, 2019 ). IL-17 promotes pathologic placental trophoblast migration, viability, and invasion via PPAR-γ/RXR-α/Wnt signaling ( Zhang et al, 2022a ).…”

“…Despite great strides over the last several decades to elucidate the placental mechanisms of neurodevelopmental disorders and PNI outcomes, this work has been limited by a number of pervasive issues. One major confound in these studies is prematurity, which itself is associated with exacerbations to the fetal neuroimmune milieu and multiple placental conditions discussed here, such as preeclampsia ( Bhati et al, 2023 ; Krishnan et al, 2013 ). Placental conditions should be considered for their impact on brain development independently from that of prematurity and other factors which are colinear with it, such as low birth weight, lung immaturity, and exposure to increased medical/environmental stress (e.g., heel stick).…”