This study by Haraguchi et al. demonstrates that maternal oral dysbiosis increases the risk of intestinal inflammation in offspring. Specifically, periodontal disease promotes the growth of oral pathobionts (e.g., Klebsiella aerogenes), which are then transmitted to the infant gut. This transmission alters gut immunity and increases susceptibility to T-cell-dependent enteritis. Although these maternally transmitted oral pathobionts are eliminated as the gut microbiota matures, the susceptibility to enteritis persists into adulthood.
Outline of this study: Mice born from dams with artificially induced periodontitis (MatOP) are prone to developing inflammatory bowel disease (CC BY-NC-ND 4.0).
The study suggests that maintaining a healthy maternal microbiota in sites other than the gut (e.g., oral cavity) is crucial for shaping a healthy offspring gut microbiota and for long-term health. It also indicates that the immature gut microbiota in infants allows for the ectopic colonization of maternally transmitted oral pathobionts, which in turn alters T-cell immunity and contributes to the exacerbation of enteritis. Cross-fostering experiments suggest that postnatal exposure to maternal oral pathobionts has a greater impact on predisposing offspring to exacerbated enteritis than maternal systemic inflammation during pregnancy. Furthermore, the study implies that the colonization of K. aerogenes alone does not worsen enteritis, suggesting that "pathogenic imprinting" from the mother plays a more significant role in inducing disease susceptibility.
