Innate and Adaptive Immunity is not Impacted by Inflammatory Bowel Disease Medications in Pregnant Women and Their Offspring.

Background and aims: Inflammatory bowel disease (IBD) therapeutics and pregnancy itself are known to impact immune cell populations, but a detailed understanding of the effect of specific therapies is lacking, particularly for infants exposed in utero. With comprehensive flow cytometric assessment, we aimed to explore how IBD and its treatment impact both maternal and infant immunophenotypes and cytokine production.

Methods: Peripheral blood was taken for flow cytometry immunophenotyping and quantification of cytokine responses to stimulation from women with IBD and healthy controls throughout pregnancy, at delivery, and postpartum. Blood samples were also taken from the umbilical cord and peripherally from the resultant offspring at the age of 6 weeks.

Results: Eighteen participants (16 with IBD and 2 healthy controls) were recruited to this single-center prospective cohort study. Basal T regulatory cell population proportions were 46% lower (0.21% vs 0.39%, P = .027) in those participants exposed to ustekinumab (n = 4). No other significant differences were noted in immunophenotype according to drug therapy exposure. Basal (1.75% vs 0.47%, P = .036) and lipopolysaccharide-stimulated (72.2% vs 64.7%, P = .028) production of tumour necrosis factor by classical dendritic cells were increased 3.7- and 1.1-fold, respectively, in those with an elevated fecal calprotectin (n = 6). Basal CD4+α4β7+ (41.4% to 66.5%, P = .0043) and CD8+α4β7+ (81.2% to 93.6%, P = .007) population proportions increased 1.6- and 1.2-fold, respectively, in infants from birth to 6 weeks.

Conclusions: This study provides the foundation for ongoing investigation to more definitively extricate the impact of maternal IBD activity, drug exposures, and disease phenotype on infant immune system development and function. These novel data suggest that IBD pharmacotherapies may not significantly impact maternal or infant immune regulation.