How Maternal Oral Microbes Raise Offspring's Risk of Gut Inflammation

Researchers from Osaka University and the University of Michigan have shown in mice that if the mother has periodontitis and oral pathogens (in particular Klebsiella aerogenes ) grow in the mouth, these microbes are transmitted to the intestines of the pups, disrupt the development of immunity and make the offspring more vulnerable to T-cell-dependent enteritis. Even when the “oral” bacteria later disappear from the intestines, the increased susceptibility to inflammation remains into adulthood. The work was published in Cell Reports.

Background

• The mouth-gut axis and inflammatory bowel disease. In recent years, evidence has accumulated that "oral" bacteria are capable of ectopically colonizing the intestine and increasing inflammation there. A classic study by Atarashi et al. showed that Klebsiella spp. strains from saliva take root in the intestine of mice, induce a Th1 response, and aggravate colitis. Reviews have noted that oral taxa are more often found in the feces of patients with IBD, and the "oral dysbiosis ↔ intestinal inflammation" relationship goes beyond individual observations.
• Periodontitis as a source of "pathobionts". Periodontitis changes the ecology of the oral cavity and expands the proportion of opportunistic enterobacteria (Klebsiella/Enterobacter, etc.). In mouse models, it was periodontitis that increased intestinal inflammation through the "migration" of these bacteria from the mouth to the intestine - the concept of intermucosal communication.
• Early microbiota “seeding”: a window of vulnerability. In the first months of life, the infant’s microbiota is formed from maternal niches (gut, vagina, skin, breast milk). Strain-stratified studies and meta-analyses show significant vertical transmission (e.g., Bifidobacterium ), especially during vaginal birth. This “imprinting” of mucosal immunity for years to come.
• The transmission of specifically “oral” microbes is a gap. Most studies on vertical transmission have focused on maternal gut strains; the role of the oral cavity as a donor of microbes to the infant gut is less well understood. Anecdotal studies have suggested “oralization” of the gut in IBD, but mechanistic data on the maternal source and long-term immune “footprint” have been lacking—a gap that the new paper addresses.
• Why postnatal contact is important. Care and feeding in the first weeks of life are the time of maximum microbial transmission. Reviews of vertical transmission emphasize the role of surrounding maternal niches and care practices; therefore, not only pregnancy but also the postnatal period is critical for “tuning” the child’s immunity.
• Context pregnancy ↔ oral health. Periodontitis in pregnant women is common and often undertreated (barriers to access/myths about dental safety). Several reviews and meta-analyses have linked maternal periodontal disease with adverse pregnancy outcomes (preterm birth, low birth weight), although the strength of the associations and the effect of treatment vary between studies. This strengthens the argument for active dental prevention in perinatal care.
• Immunological perspective. “Oral” enterobacteria of the Klebsiella type are able to bypass local immunity and, against the background of inflammation, more easily establish themselves in the intestine; in models, this leads to T-cell inflammatory responses and a more severe course of enteritis. Therefore, the source of the microbe (the mother’s oral cavity) and the time of encounter (early infancy) are key determinants of risk.
• What the current work adds. The Cell Reports authors trace for the first time the pathway: maternal periodontitis → growth of oral pathobionts ( Klebsiella aerogenes ) → transmission to the child's gut in postnatal contact → long-term increased susceptibility to T-cell-dependent enteritis, even when these oral bacteria are no longer visible in the microbiota. This elevates dental prophylaxis in pregnancy/lactation from a "local" task to a factor in systemic child health.

What did the scientists do?

• Periodontitis was modeled in females (ligature model), which resulted in the growth of opportunistic bacteria in the mouth, including K. aerogenes. These “oral” microbes then colonized the intestines of newborns – as early “pioneers” of their microbiota.
• They checked how such early settlement affects inflammatory bowel diseases: pups from mothers with periodontitis suffered from T-cell-dependent enteritis more severely than controls.
• Cross-fostering was performed (the litters were exchanged): it turned out that postnatal contact with maternal oral pathobionts is more important than systemic maternal inflammation during pregnancy. In other words, it was the early life that was decisive - feeding/care in the first weeks.
• An important detail: colonization by K. aerogenes alone without the “maternal context” is not enough to increase enteritis. The authors talk about “pathogenic imprinting” — a complex trace of early interactions with maternal microbes.

Why is this important?

We are used to discussing the influence of the mother's gut microbiota on the child. This work shifts the focus: non-intestinal microbial niches - primarily the oral cavity - can also format the immunity of the newborn and set long-term risks. In experiments, the infant gut turned out to be "hospitable" to "foreign" oral bacteria; they temporarily took root, shifted T-cell responses, and the trace (increased susceptibility to enteritis) remained even after they left.

What exactly was shown on the models

• Mouth-to-gut transmission: In maternal periodontitis, oral pathobionts, including K. aerogenes, were transferred to the pups and became part of their early microbiota.
• Mucosal immune 'rewiring': Early oral colonization altered the T-cell landscape in the offspring's gut, leading to greater inflammation when challenged.
• Long trail: although as the puppies “grew up,” the microbiota was cleared of oral invaders, the predisposition to enteritis did not disappear, which indicates the effect of early imprinting of immunity.

How to "translate" this to people - carefully

This is work on mice, so it’s too early to draw direct clinical conclusions. But it reinforces the idea of a mouth-gut axis and adds a practical hint: the oral health of an expectant mother may be about more than just her teeth and gums, but also about the child’s microbial “hereditary baggage.” Parallel clinical observations have already linked periodontitis in pregnant women with adverse outcomes in children, and now a mechanistic link to the gut is emerging.

What can be done now

• Screening and treatment of periodontitis before and during pregnancy (in collaboration with a dentist/periodontist). This is not a “treatment for baby colitis,” but a sensible hygiene measure with other proven benefits.
• Oral hygiene and regular check-ups are basic prevention that does not have the side effects of systemic therapy.
• Feeding/care in the early postnatal period is the source of the closest microbial contact. The authors show that it is postnatal transmission in the first weeks of life that may be decisive.

Limitations and questions for the future

• Model nature of the data: mice ≠ humans; prospective cohort and intervention studies in humans (including maternal/infant microbiome, mucosal immune markers) are needed.
• Which oral bacteria are “dangerous”? The paper mentions K. aerogenes, but the clinical spectrum is broader; “pathobiont signatures” and their transmission windows need to be mapped.
• Is it possible to “rewire” the risk? Research on probiotic/prebiotic interventions in mothers with periodontitis, as well as dental sanitation protocols during pregnancy with assessment of immune outcomes in children, are promising.

Source: Haraguchi M. et al. Transmission of maternal oral pathobionts to the infant gut predisposes offspring to exacerbated enteritis. Cell Reports 44(7):115974. DOI: 10.1016/j.celrep.2025.115974