Publicação
Substance P antagonist improves both obesity and asthma in a mouse model
| dc.contributor.author | Ramalho, R. | |
| dc.contributor.author | Almeida, Joana | |
| dc.contributor.author | Beltrão, M. | |
| dc.contributor.author | Pirraco, A. | |
| dc.contributor.author | Costa, R. | |
| dc.contributor.author | Sokhatska, O. | |
| dc.contributor.author | Guardão, L. | |
| dc.contributor.author | Palmares, C. | |
| dc.contributor.author | Guimarães, J. T. | |
| dc.contributor.author | Delgado, L. | |
| dc.contributor.author | Moreira, A. | |
| dc.contributor.author | Soares, R. | |
| dc.date.accessioned | 2021-09-28T09:00:01Z | |
| dc.date.available | 2021-09-28T09:00:01Z | |
| dc.date.issued | 2012-11 | |
| dc.description.abstract | Evidence suggests a causal relationship between obesity and asthma; however, the underlying mechanisms remain unknown. Substance P (SP), involved in neurogenic inflammation by acting through its receptor NK1-R, seems to participate in obese–asthma phenotype in mice. To evaluate the effect of a selective substance P receptor antagonist on a mouse model of diet-induced obesity and asthma. Diet-induced obese Balb/c mice were sensitized and challenged with ovalbumin (OVA) and treated with a selective NK1-R antagonist or placebo. Serum glucose, insulin, IL-6, resistin, and OVA-specific IgE levels were quantified. A score for peribronchial inflammation in lung histology was used. Cells were counted in bronchoalveolar lavage fluid. Adipocyte sizes were measured. Ovalbumin-obese mice treated with NK1-R antagonist had lower weight (P = 0.0002), reduced daily food intake (P = 0.0021), reduced daily energy intake (P = 0.0021), reduced surface adipocyte areas (P < 0.0001), lower serum glucose (P = 0.04), lower serum insulin (P = 0.03), lower serum IL-(P = 0.0022), lower serum resistin (P = 0.0043), lower serum OVA-specific IgE (P = 0.035), and lower peribronchial inflammation score (P < 0.0001) than nontreated OVA-obese mice. We observed an interaction between obesity, allergen sensitization, and treatment with NK1-R antagonist for metabolic and systemic biomarkers, and for allergen sensitization and bronchial inflammation, showing a synergy between these variables. In an experimental model of obesity and asthma in mice, NK1-R blockade improved metabolic and systemic biomarkers, as well as allergen sensitization and bronchial inflammation. These positive effects support a common pathway in the obese–asthma phenotype and highlight SP as a target with potential clinical interest in the obese–asthma epidemics. | pt_PT |
| dc.description.version | info:eu-repo/semantics/publishedVersion | pt_PT |
| dc.identifier.citation | Ramalho, R., Almeida, J., Beltrão, M., Pirraco, A., Costa, R., Sokhatska, O., Guardão, L., Palmares, C., Guimarães, J. T., Delgado, L., Moreira, A., & Soares, R. (2013). Substance P antagonist improves both obesity and asthma in a mouse model. Allergy, 68(1), 48-54. https://doi.org/https://doi.org/10.1111/all.12052 | pt_PT |
| dc.identifier.doi | 10.1111/all.12052 | pt_PT |
| dc.identifier.issn | 1398-9995 | |
| dc.identifier.uri | http://hdl.handle.net/10400.22/18592 | |
| dc.language.iso | eng | pt_PT |
| dc.peerreviewed | yes | pt_PT |
| dc.publisher | Wiley | pt_PT |
| dc.relation.publisherversion | https://onlinelibrary.wiley.com/doi/10.1111/all.12052 | pt_PT |
| dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | pt_PT |
| dc.subject | Animal model | pt_PT |
| dc.subject | Asthma | pt_PT |
| dc.subject | NK1-R antagonist | pt_PT |
| dc.subject | Obesity | pt_PT |
| dc.subject | Substance P | pt_PT |
| dc.subject | Treatment | pt_PT |
| dc.title | Substance P antagonist improves both obesity and asthma in a mouse model | pt_PT |
| dc.type | journal article | |
| dspace.entity.type | Publication | |
| oaire.citation.endPage | 54 | pt_PT |
| oaire.citation.startPage | 48 | pt_PT |
| oaire.citation.title | Allergy | pt_PT |
| oaire.citation.volume | 68 | pt_PT |
| person.familyName | ALMEIDA | |
| person.givenName | JOANA | |
| person.identifier.ciencia-id | 1317-637D-8EE0 | |
| person.identifier.orcid | 0000-0001-8043-9053 | |
| rcaap.rights | openAccess | pt_PT |
| rcaap.type | article | pt_PT |
| relation.isAuthorOfPublication | 5ec466aa-7e58-47b6-a45b-b9ee3e6f6552 | |
| relation.isAuthorOfPublication.latestForDiscovery | 5ec466aa-7e58-47b6-a45b-b9ee3e6f6552 |
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