CHILDREN with persistent food allergy were found to have distinct placental DNA methylation and inflammatory profiles, with reduced interleukin (IL)-10 and elevated T helper 2 (Th2) cytokines associated with an early persistent disease trajectory.
Researchers analysed data from 1,518 children participating in the COCOA study, who were followed until seven years of age. Food allergy trajectories were classified using group-based trajectory modelling, while serum cytokines were measured at three and seven years. Placental DNA methylation was also assessed using the Infinium MethylationEPIC BeadChip.
Four food allergy trajectories were identified: no food allergy in 87.3% of children, early remission in 6.9%, early persistent food allergy in 4.6%, and late remission in 1.1%.
Children in the early persistent food allergy trajectory had higher levels of IL-4, IL-5, and IL-6 at both three and seven years compared with children who did not develop food allergy.
At three years, IL-10 levels were lower among children with early persistent food allergy than among those following a late remission trajectory. IL-10 is involved in regulating immune responses, while IL-4 and IL-5 are associated with type 2 immune responses.
The findings therefore identified differences in inflammatory profiles between children whose food allergy persisted early in childhood and those without food allergy or with later remission.
Placental DNA methylation analysis identified significant hypermethylation of the RPS6KA2 and GCSAML genes among children with early persistent food allergy compared with those in the no food allergy and early remission trajectories.
Methylation of GCSAML was positively associated with total immunoglobulin E, egg white-specific immunoglobulin E, early-life eosinophil levels, and IL-5 concentrations at seven years. All associations reached statistical significance at p<0.05.
The researchers concluded that hypermethylation of RPS6KA2 and GCSAML, alongside reduced IL-10 and elevated Th2 cytokines, was associated with an early persistent food allergy trajectory.
These findings suggest that placental epigenetic alterations and immune dysregulation may contribute to the development and persistence of food allergy in childhood. Further research will be needed to establish whether these biological changes play a causal role in determining food allergy trajectories.
Reference
Choi EJ et al. Placental epigenetic alterations and IL-10 dysregulation drive early persistent food allergy. Allergy. 2026;DOI:10.1111/all.70471.
Featured image: Microgen on Adobe Stock.
Each article is made available under the terms of the Creative Commons Attribution-Non Commercial 4.0 License.
