Evidence map›Paper›PMID 41590514›Full record

ReviewJournal of personalized medicine2026

Connecting the Airways: Current Trends in United Airway Diseases.

Benedetta Bondi, Martina Buscema, Federico Di Marco, Carlo Conti, Andrea Caviglia, Lorenzo Fucci, Anna Maria Riccio, Marcello Mincarini, Martina Ottoni, Fulvio Braido and 2 more

Abstract readReview
In one paragraph

Review in Journal of personalized medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Benedetta BondiRespiratory and Allergy Clinic, IRCCS Ospedale Policlinico San Martino, 16132 Genoa, Italy.
Martina BuscemaRespiratory and Allergy Clinic, IRCCS Ospedale Policlinico San Martino, 16132 Genoa, Italy.
Federico Di MarcoRespiratory and Allergy Clinic, IRCCS Ospedale Policlinico San Martino, 16132 Genoa, Italy.
Carlo ContiENT Department, IRCCS Policlinico San Martino, University of Genoa, 16132 Genoa, Italy.ORCID 0009-0005-5933-2936
Andrea CavigliaENT Department, IRCCS Policlinico San Martino, University of Genoa, 16132 Genoa, Italy.
Lorenzo FucciENT Department, IRCCS Policlinico San Martino, University of Genoa, 16132 Genoa, Italy.
Anna Maria RiccioRespiratory and Allergy Clinic, IRCCS Ospedale Policlinico San Martino, 16132 Genoa, Italy.
Marcello MincariniRespiratory and Allergy Clinic, IRCCS Ospedale Policlinico San Martino, 16132 Genoa, Italy.
Martina OttoniAllergy and Clinical Immunology, Medicine and Surgery Department, University of Parma, 43121 Parma, Italy.ORCID 0009-0004-5287-4620
Fulvio BraidoRespiratory and Allergy Clinic, IRCCS Ospedale Policlinico San Martino, 16132 Genoa, Italy.
Rikki Frank CanevariENT Department, IRCCS Policlinico San Martino, University of Genoa, 16132 Genoa, Italy.ORCID 0000-0002-1821-7262
Diego BagnascoRespiratory and Allergy Clinic, IRCCS Ospedale Policlinico San Martino, 16132 Genoa, Italy.ORCID 0000-0002-3661-5731

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The concept of united airway disease (UAD) highlights the bidirectional relationship between inflammatory disorders of the upper airways-such as allergic rhinitis and chronic rhinosinusitis with or without nasal polyps (CRSwNP/CRSsNP)-and lower airway diseases, most notably asthma. This paradigm is supported by epidemiological, embryological, and immunological evidence demonstrating that airway inflammation represents a single, interconnected process rather than isolated compartmental pathology. Central to many UAD phenotypes is type 2 (T2) inflammation, driven by cytokines including IL-4, IL-5, and IL-13, and mediated by effector cells such as eosinophils and group 2 innate lymphoid cells (ILC2s). Epithelial barrier dysfunction often serves as the initiating trigger for this shared inflammatory cascade by production of TSLP, IL-25 and IL-33. Optimal diagnosis and management of UAD require an integrated, multidisciplinary framework. Clinical evaluation remains essential for patient characterization but must be complemented by pheno-endotypic assessment using imaging (CT), allergy testing, biomarker profiling (FeNO, blood eosinophils, IgE), and pulmonary function testing (spirometry, impulse oscillometry). Therapeutic strategies are layered, targeting both symptom control and inflammation across airway compartments. Standard approaches include intranasal and inhaled corticosteroids as well as saline irrigations, while severe T2-high disease increasingly benefits from biologic therapies (anti-IL-5/IL-5R, anti-IL-4R, anti-TSLP), which reduce dependence on systemic corticosteroids and surgical interventions such as endoscopic sinus surgery (ESS). Emerging precision-medicine models, particularly the "treatable traits" approach, further underscore the need to view the airway as a unified system. Collectively, these insights reinforce the clinical imperative of addressing upper and lower airway disease as a continuum, ensuring that inflammation in one district is neither overlooked nor treated in isolation.

Indexed as

biologic therapytype 2 inflammationunited airway disease (UAD)

Identifiers

PMID41590514
PMCPMC12843504

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.