Allergic Rhinitis Reshapes the Nasopharyngeal Microbiome and Metabolome in Children With Severe Adenoid Hypertrophy

Adenoid hypertrophy, the abnormal enlargement of the lymphoid tissue at the back of the nasal cavity, affects between roughly 12 and 34 percent of children and is one of the most common reasons for pediatric ear, nose, and throat surgery. Yet a growing body of evidence suggests that the condition rarely exists in isolation. Children with allergic rhinitis, an IgE-mediated hypersensitivity of the nasal mucosa that affects an estimated 2 to 25 percent of children worldwide, appear far more likely to develop enlarged adenoids than their non-allergic peers. A new study published in Frontiers in Medicine now offers a molecular explanation for that clinical overlap, showing that allergy leaves a measurable fingerprint on both the bacterial communities and the metabolic chemistry of the adenoid surface.

Researchers at Wuhan Third Hospital in China recruited 18 children with grade IV adenoid hypertrophy, the most severe category of nasopharyngeal obstruction, between August and November 2024. Nine of the children also carried a diagnosis of allergic rhinitis, while nine did not. The team deliberately excluded children with tonsillar disease, recent respiratory infections, recent use of nasal steroids, antihistamines, or antibiotics, household smoking, pets, and unusual diets, in an effort to isolate the effect of allergy alone. Serum total IgE and reflective total nasal symptom scores were significantly higher in the allergic group, confirming the clinical distinction between the two cohorts, while age, sex, body mass index, and routine blood counts were statistically comparable.

To profile the microbial landscape, the investigators collected adenoid surface secretions under general anesthesia using sterile swabs rotated five times across the tissue, taking care to avoid contamination from the oral mucosa or saliva. Bacterial DNA was then extracted and the 16S rDNA V3-V4 region was amplified and sequenced on an Illumina NovaSeq platform, a culture-independent technique that captures organisms conventional cultivation misses. In parallel, the team performed untargeted metabolomics using ultra-performance liquid chromatography coupled with high-resolution tandem mass spectrometry, annotating compounds against the KEGG and HMDB databases.

The sequencing results revealed a striking shift in community structure. Children with allergic rhinitis showed significantly higher alpha diversity, measured by both the Chao1 richness index and the Shannon index, indicating a richer and more varied bacterial population on the adenoid surface. Principal coordinate analysis based on weighted UniFrac distances confirmed that the overall composition of the microbiota differed significantly between the two groups, with a statistical separation that was highly significant. At the phylum level, Firmicutes dominated the adenoids of children without allergy, whereas Fusobacteriota and Actinobacteriota took precedence in the allergic group.

Among the top twenty differentially abundant genera, three stood out: Fusobacterium, Actinomyces, and Veillonella were all significantly enriched in children with allergic rhinitis. Linear discriminant analysis effect size analysis reinforced these differences across every taxonomic level from phylum to species. The authors note that these same genera have been previously identified among the fifteen microbial communities characteristic of the nasopharynx, but their dominance in allergic children suggests that IgE-driven inflammation may actively reshape which bacteria colonize the adenoid biofilm.

The metabolomic analysis was equally revealing. Of the 706 metabolites identified across the 18 samples, 255 changed significantly between groups, with 140 reduced and 115 increased in the allergic cohort. Partial least squares discriminant analysis cleanly separated the two groups, and KEGG pathway enrichment pointed to twelve metabolic pathways that were significantly altered, including the biosynthesis and degradation of branched-chain amino acids such as valine, leucine, and isoleucine, the pentose phosphate pathway, glycine, serine, and threonine metabolism, aromatic amino acid biosynthesis, galactose and fructose metabolism, histidine metabolism, vitamin B6 metabolism, unsaturated fatty acid biosynthesis, and glycerophospholipid metabolism.

Perhaps the most intriguing finding came from the integration of the two datasets. Spearman correlation analysis between the three differential bacterial genera and thirty differential metabolites revealed a dense web of significant associations. Fusobacterium correlated positively with eleven metabolites and negatively with five, Veillonella correlated positively with ten and negatively with two, and Actinomyces correlated positively with fourteen and negatively with eleven. These patterns suggest that the allergic inflammatory environment does not merely change which bacteria are present but also alters what those bacteria produce, creating a feedback loop in which microbial metabolites may further stimulate adenoid immune activation and tissue growth.

The clinical implications are considerable. Adenoidectomy remains the standard treatment for severe disease, but it carries risks of bleeding and infection, and roughly 13 to 15 percent of children require a second procedure because of regrowth. Some researchers have argued that surgery offers no clear benefit for the majority of children who have both allergic rhinitis and adenoid hypertrophy. If the three bacterial genera identified here prove to be reliable biomarkers, they could eventually support non-invasive diagnosis through nasopharyngeal swabs and guide targeted anti-allergic or microbiome-directed therapies before surgery becomes necessary.

The authors are careful to acknowledge the limitations of their work. The sample size is small, the cohort was drawn from a single tertiary center rather than the general population, and the observed correlations between microbes and metabolites do not establish causation. Future studies using microbiota transplantation or longitudinal sampling will be needed to confirm whether the allergic microbiome actively drives adenoid enlargement or simply accompanies it. Nevertheless, the study provides a compelling molecular framework for a clinical observation that has puzzled pediatricians for decades, and it opens a concrete path toward interventions that target the nasopharyngeal ecosystem rather than the tissue alone.

Subject of Research: The effect of allergic rhinitis on nasopharyngeal microbiota and metabolomics in children with severe adenoid hypertrophy

Article Title: The impact of allergic rhinitis on nasopharyngeal microbiota and metabolomics in children with severe adenoid hypertrophy

Article References: Wang, B., Chen, T., Gao, S., Jin, H., Liang, G., Gong, G., & Xiao, L. (2026). The impact of allergic rhinitis on nasopharyngeal microbiota and metabolomics in children with severe adenoid hypertrophy. Frontiers in Medicine, 13, Article 1895589. https://doi.org/10.3389/fmed.2026.1895589

Image Credits: AI Generated

DOI: 10.3389/fmed.2026.1895589

Keywords: allergic rhinitis, adenoid hypertrophy, pediatric otolaryngology, microbiome, metabolomics, 16S rDNA sequencing, nasopharyngeal microbiota, IgE, impact, allergic, rhinitis, nasopharyngeal