Distinction between rhinitis alone and rhinitis with asthma using interactomics
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Author
Aguilar, D.Lemonnier, N.
Melén, E.
Bustamante, M.
Gruzieva, O.
Guerra, S.
Keil, T.
Koppelman, G.H.
Celedón, J.C.
Antó, J.M.
Bousquet, J.
Affiliation
Asthma and Airway Disease Research Center, University of ArizonaIssue Date
2023-08-12
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Nature ResearchCitation
Aguilar, D., Lemonnier, N., Melén, E. et al. Distinction between rhinitis alone and rhinitis with asthma using interactomics. Sci Rep 13, 13125 (2023). https://doi.org/10.1038/s41598-023-39987-6Journal
Scientific ReportsRights
© The Author(s) 2023. This article is licensed under a Creative Commons Attribution 4.0 International License.Collection Information
This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.Abstract
The concept of “one-airway-one-disease”, coined over 20 years ago, may be an over-simplification of the links between allergic diseases. Genomic studies suggest that rhinitis alone and rhinitis with asthma are operated by distinct pathways. In this MeDALL (Mechanisms of the Development of Allergy) study, we leveraged the information of the human interactome to distinguish the molecular mechanisms associated with two phenotypes of allergic rhinitis: rhinitis alone and rhinitis in multimorbidity with asthma. We observed significant differences in the topology of the interactomes and in the pathways associated to each phenotype. In rhinitis alone, identified pathways included cell cycle, cytokine signalling, developmental biology, immune system, metabolism of proteins and signal transduction. In rhinitis and asthma multimorbidity, most pathways were related to signal transduction. The remaining few were related to cytokine signalling, immune system or developmental biology. Toll-like receptors and IL-17-mediated signalling were identified in rhinitis alone, while IL-33 was identified in rhinitis in multimorbidity. On the other hand, few pathways were associated with both phenotypes, most being associated with signal transduction pathways including estrogen-stimulated signalling. The only immune system pathway was FceRI-mediated MAPK activation. In conclusion, our findings suggest that rhinitis alone and rhinitis and asthma multimorbidity should be considered as two distinct diseases. © 2023, Springer Nature Limited.Note
Open access journalISSN
2045-2322PubMed ID
37573373Version
Final Published Versionae974a485f413a2113503eed53cd6c53
10.1038/s41598-023-39987-6
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Except where otherwise noted, this item's license is described as © The Author(s) 2023. This article is licensed under a Creative Commons Attribution 4.0 International License.

