Probiotic Oral Spray for Enlarged Adenoids: What It Changed
A five-month trial changed upper-airway microbiota in children with enlarged adenoids, but did not test sleep, symptoms, adenoid size, or surgery.
A probiotic oral spray changed the pharyngeal and nasal microbiota of children with adenotonsillar hypertrophy. It did not show that their adenoids shrank, their sleep improved, or that they avoided surgery. That distinction is the whole story.
In a 2024 double-blind, placebo-controlled randomized trial, children aged 3 to 8 with grade II–IV adenotonsillar hypertrophy who were awaiting surgery used a spray containing Streptococcus salivarius 24SMBc and Streptococcus oralis 89a twice daily for five months. The spray contained at least 125 × 109 CFU/g combined. Compared with placebo, treatment shifted microbial community composition in pharyngeal and nasal samples and reduced the abundance of several pathobionts. Those are real, disease-relevant biological findings. They are also surrogate outcomes, not evidence of clinical benefit.
The trial changed the target, not the outcome patients feel
Del Chierico et al.'s 2024 randomized trial tested whether a locally delivered probiotic could alter upper-airway microbial ecology in children with substantial disease. That was a sensible question. Adenotonsillar hypertrophy is common in childhood and often leads to surgery because enlarged adenoids and tonsils can contribute to nasal obstruction, recurrent inflammation, and sleep-disordered breathing.
The researchers enrolled children already on a surgical waitlist, used placebo and blinding, and followed participants for five months. They collected pharyngeal and nasal samples and used 16S rRNA metataxonomic sequencing, which characterizes bacterial communities more broadly than conventional culture. Clinical visits at months 1, 3, and 5 recorded acute and chronic inflammation signs, body temperature, and drug consumption. The investigators also evaluated season as a possible influence on the microbiome.
The active spray altered community structure at both sampled sites relative to placebo. It also reduced pathobionts implicated in adenotonsillar disease and recurrent upper-respiratory infections, including Haemophilus influenzae, Streptococcus mitis, and Gemella haemolysans. The publication supports the conclusion that this intervention can modify the upper-airway microbiome during active treatment.
It does not support the conclusion that the spray treats adenotonsillar hypertrophy. The study did not measure adenoid size by imaging or endoscopy, sleep by polysomnography or apnea–hypopnea index, symptom burden with a validated questionnaire, or the rate at which children proceeded to surgery. A more favorable bacterial profile may matter clinically, but this trial did not establish that link.
Why the microbiome finding is still interesting
The delivery route fits the hypothesis. The two strains are commensal streptococci associated with the oropharyngeal mucosa, and the spray placed them near the anatomical sites under study. A related but separate line of evidence makes the general route plausible: in a human randomized trial, De Boeck et al. reported in 2025 that a chewable formulation of Lacticaseibacillus rhamnosus GG colonized the nasal mucosa and produced local immune benefits in people with allergic rhinoconjunctivitis.
That study does not validate the adenotonsillar spray. It used a different strain, a different formulation, and a different patient population. Still, it helps answer a narrower question: can an orally administered probiotic influence the upper airway rather than merely pass through the gut? Human evidence says it can.
The adenoid microbiome also gives the intervention a biologically credible target. A 2026 review by Sokolovs-Karijs et al. describes the adenoid surface as a bacterial reservoir associated with adenotonsillar hypertrophy and otitis media with effusion. Association is not proof that bacteria cause the enlargement, and it certainly does not prove that replacing bacteria reverses it. But it explains why researchers would test a topical microbial intervention in the first place.
The missing surrogate validation problem
The field has not identified a microbial signature that reliably predicts a child will breathe better, sleep better, or need less surgery. That makes pathobiont reduction an unvalidated surrogate endpoint. A change in bacterial abundance can be statistically detectable and biologically plausible while having little or no effect on a patient's symptoms.
A 2026 narrative review of the pediatric nasal microbiome by Sîrbu et al. reaches the appropriately cautious conclusion: researchers still lack consensus on sampling methods, microbial thresholds, and consistent links between microbiota patterns and specific pediatric ENT disorders. This is not a minor technical loose end. Without a validated bridge between sequencing results and clinical outcomes, the magnitude of benefit from microbiome remodeling remains unknown.
Season adds another complication. Upper-airway microbial communities vary over time, and the trial appropriately considered seasonal variation as a confounder. That analysis strengthens the study's design, but it cannot make all ecological variation disappear. The observed treatment-associated shifts may include some contribution from background seasonal change.
Antibiotics may test durability in the real world
Children with severe adenotonsillar disease can receive antibiotics for recurrent infections during a five-month treatment period. That matters because antibiotic exposure can disrupt the microbial community a probiotic is trying to reshape. A 2024 systematic review by Łukasik et al. found limited evidence that probiotics restore microbiota to its pre-antibiotic state after antibiotic-induced disruption.
The review did not study this oral spray or children with adenotonsillar hypertrophy, so it cannot determine whether antibiotics erased the trial's effects. It does raise a practical question for follow-up studies: do the pharyngeal and nasal changes persist through antibiotic courses, and do they remain after the twice-daily spray stops? The five-month trial measured the microbiome while treatment continued, not after discontinuation.
Why gut-probiotic evidence does not settle this question
Probiotics have been studied much more extensively for gut-related and systemic outcomes than for upper-airway microbial therapy. For example, a 2025 meta-analysis of pediatric atopic dermatitis trials evaluated probiotic effects on eczema severity, while a 2025 Cochrane review assessed probiotics and synbiotics for preventing allergic disease in infants. Those evidence bases concern different strains, routes, age groups, tissues, and outcomes.
A probiotic is not a class effect in a bottle. A finding for an intestinal intervention cannot establish that two specific oral streptococcal strains will colonize the pharynx, reduce adenoid size, or improve obstructive symptoms.
What should happen next
The next trial needs to preserve the current study's strengths—randomization, placebo control, blinding, repeated sampling, and adequate treatment duration—while adding outcomes that matter to children and families. These include standardized adenoid grading, validated symptom measures, sleep-disordered-breathing assessments, antibiotic exposure, persistence after treatment stops, and surgery rates.
The spray has earned a place in the research pipeline, not in a treatment plan for avoiding adenoid surgery.
For now, the evidence supports a narrow conclusion: topical commensal bacteria can reshape upper-airway microbiota in children with severe adenotonsillar hypertrophy over five months. Whether that microbial shift changes the disease remains unanswered.
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