Garcia-Flores V, Romero R, Furcron AE, Levenson D, Galaz J, Zou C, Hassan SS, Hsu CD, Olson D, Metz G, Gomez-Lopez N.
Front Immunol. 2020 Feb 26;11(254). doi: 10.3389/fimmu.2020.00254.
Maternal stress is a well-established risk factor for preterm birth and has been associated with adverse neonatal outcomes in the first and subsequent generations, including increased susceptibility to disease and lasting immunological changes. However, a causal link between prenatal maternal stress and preterm birth, as well as compromised neonatal immunity, has yet to be established. To fill this gap in knowledge, PRB researchers developed a murine model of prenatal maternal stress across three generations and high-dimensional flow cytometry to evaluate neonatal adaptive immunity.
The team reported that recurrent prenatal maternal stress induced preterm birth in the first and second filial generations and negatively affected early neonatal growth. Strikingly, prenatal maternal stress induced a systematic reduction in T cells and B cells, the former including regulatory CD4+ T cells as well as IL-4- and IL-17A-producing T cells, in the second generation. Yet, neonatal adaptive immunity gained resilience against prenatalmaternal stress by the third generation. The team also showed that the rate of prenatal maternal stress-induced preterm birth can be reduced upon cessation of stress, though neonatal growth impairments persisted. These findings provide evidence that prenatal maternal stress causes preterm birth and affects neonatal immunity across generations, adverse effects that can be ameliorated upon cessation.