Publication
Editorial comments on “Multiarray screening identifies plasma proteins associated with Th17 cell differentiation and viral defense in coincident asthma and obesity”
| dc.contributor.author | Rufo, João Cavaleiro | |
| dc.contributor.author | Chauhan, Jitesh | |
| dc.contributor.author | Kalayci, Ömer | |
| dc.contributor.author | Eigenmann, Philippe | |
| dc.contributor.author | Cavaleiro Rufo, João | |
| dc.date.accessioned | 2025-12-23T15:05:44Z | |
| dc.date.available | 2025-12-23T15:05:44Z | |
| dc.date.issued | 2024-09 | |
| dc.description.abstract | The clinical associations between asthma and obesity remain poorly understood. The increasing prevalence ofboth conditions occurring may represent a modern clinical paradox. It is unclear whether reduced physical activ-ity in children with asthma leads to obesity, or if asthma-like symptoms in obese children result directly from theassociated excessive abdominal fat, impaired lung function, and heightened Th2 inflammation. Determining theetiology of both diseases and their interconnection is therefore an important research avenue.A recent study has sought to investigate this through a cross-sectional analysis of Australian children, bothwith and without asthma, examining their levels of physical activity. Interestingly, the study found no evidencethat asthma hindered physical activity.1 On the other hand, although most studies have shown obesity is linkedto a higher risk of asthma, the exact mechanism remains unclear. Many studies refer to obesity as an exacerbationfactor for asthma symptoms rather than a direct contributor to the underlying pathophysiological mechanisms ofasthma. 2 This highlights the need for continued research to untangle the complex interplay between these twoconditions.In 2019, a study investigating the associations between exposure to endocrine-disrupting chemicals andchildhood asthma identified a specific pattern of volatile organic compounds that were significantly linked to theearly onset “obese-asthma” phenotype, but not to asthma or obesity independently. 3 This suggests that asthmaand obesity may share common risk factors that trigger disease onset of both conditions during early childhood.Supporting this hypothesis, subsequent research has identified 29 genes associated with the obese-asthma phe-notypes, including GBP5 and SOCS, which further highlights the genetic underpinnings of this dual condition. 4In this issue, Manell et al. offer valuable insights by investigating novel plasma protein biomarkers specificallyassociated with the coexistence of asthma and obesity in an adolescent population. 5 The cross-sectional studyinvolved 390 children and adolescents, aged 10 to 19, who were categorized into four groups: healthy controls,individuals with asthma, individuals with obesity, and those with both obesity and asthma (OA).A proximity extension assay was used to assess the relative plasma concentrations of 113 proteins associatedwith inflammation and immune response. The study identified five plasma proteins—CCL8, IL-33, IL-17C, FGF-23,and CLEC7A—that were significantly and specifically elevated in the OA group compared to controls. However,after adjusting for age, sex, and sIgE levels, only CCL8 and CLEC7A remained significantly elevated. This suggeststhat the high levels observed for IL-33, IL-17C, and FGF-23 in the OA group may be partially attributable to atopy.Drawing on previously published evidence and considering the role of CCL8 in mucosal chemotaxis and Th2inflammation, Manell et al. propose that viral defense at mucosal barriers may play an important role in obesity-related asthma in children and adolescents. 5 While the exact pathophysiological mechanism behind CCL8 over-expression remains unclear, it is noteworthy that prior studies have confirmed no association between CCL8and atopy. 6 This, along with the evidence that CCL8 levels are regulated in obese individuals without asthma,strengthens the argument for this chemokine as a promising biomarker for obese-asthma phenotypes.Additionally, FGF-23, IL-17C, and IL-33, which are linked to mucosal host defense against viral infections andTh17 cell activation, were also regarded as potential biomarkers for concomitant asthma and obesity, though toa lesser extent. 5 Conversely, the elevated levels of CLEC7A in the OA group appear to be additive, reflecting thecombined effects of asthma and obese observed separately. | eng |
| dc.identifier.citation | Cavaleiro Rufo, J., Chauhan, J., Kalayci, Ö., & Eigenmann, P. (2024). Editorial comments on “Multiarray screening identifies plasma proteins associated with Th17 cell differentiation and viral defense in coincident asthma and obesity”. Pediatric Allergy and Immunology, 35(9), e14242. https://doi.org/10.1111/pai.14242 | |
| dc.identifier.doi | 10.1111/pai.14242 | |
| dc.identifier.eissn | 1399-3038 | |
| dc.identifier.issn | 0905-6157 | |
| dc.identifier.uri | http://hdl.handle.net/10400.22/31349 | |
| dc.language.iso | eng | |
| dc.peerreviewed | yes | |
| dc.publisher | Wiley | |
| dc.relation.hasversion | https://onlinelibrary.wiley.com/doi/10.1111/pai.14242 | |
| dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | |
| dc.subject | Obesity-asthma relationship | |
| dc.subject | Cohesive pathophysiological | |
| dc.subject | Obese-asthma phenotypes | |
| dc.title | Editorial comments on “Multiarray screening identifies plasma proteins associated with Th17 cell differentiation and viral defense in coincident asthma and obesity” | eng |
| dc.type | editorial | |
| dspace.entity.type | Publication | |
| oaire.citation.issue | 9 | |
| oaire.citation.title | Pediatric Allergy and Immunology | |
| oaire.citation.volume | 35 | |
| oaire.version | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |
| person.familyName | Cavaleiro Rufo | |
| person.givenName | João | |
| person.identifier | R-00F-QED | |
| person.identifier.ciencia-id | 0F14-AD98-862F | |
| person.identifier.orcid | 0000-0003-1175-242X | |
| person.identifier.rid | K-7994-2013 | |
| person.identifier.scopus-author-id | 56549851500 | |
| relation.isAuthorOfPublication | 762b2c6e-6710-4061-bc68-74084b460ccf | |
| relation.isAuthorOfPublication.latestForDiscovery | 762b2c6e-6710-4061-bc68-74084b460ccf |