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dc.contributor.author | Fernandez-Gallego, Nieves | |
dc.contributor.author | Castillo-Gonzalez, Raquel | |
dc.contributor.author | Moreno-Serna, Lucía | |
dc.contributor.author | García-Cívico, Antonio J | |
dc.contributor.author | Sánchez-Martínez, Elisa | |
dc.contributor.author | López-Sanz, Celia | |
dc.contributor.author | Fontes, Ana Luiza | |
dc.contributor.author | Pimentel, Lígia L | |
dc.contributor.author | Gradillas, Ana | |
dc.contributor.author | Obeso, David | |
dc.contributor.author | Neuhaus, René | |
dc.contributor.author | Ramírez-Huesca, Marta | |
dc.contributor.author | Ruiz-Fernández, Ignacio | |
dc.contributor.author | Nuñez-Borque, Emilio | |
dc.contributor.author | Carrasco, Yolanda R | |
dc.contributor.author | Ibáñez, Borja | |
dc.contributor.author | Martin, Pilar | |
dc.contributor.author | Blanco, Carlos | |
dc.contributor.author | Barbas, Coral | |
dc.contributor.author | Barber, Domingo | |
dc.contributor.author | Rodríguez-Alcalá, Luis M | |
dc.contributor.author | Villaseñor, Alma | |
dc.contributor.author | Esteban, Vanesa | |
dc.contributor.author | Sanchez-Madrid, Francisco | |
dc.contributor.author | Jiménez-Saiz, Rodrigo | |
dc.date.accessioned | 2024-07-02T09:46:49Z | |
dc.date.available | 2024-07-02T09:46:49Z | |
dc.date.issued | 2024-06-12 | |
dc.identifier.citation | Allergy. 2024 Jun 12. | es_ES |
dc.identifier.uri | http://hdl.handle.net/20.500.12105/19899 | |
dc.description.abstract | BACKGROUND Allergic diseases begin early in life and are often chronic, thus creating an inflammatory environment that may precede or exacerbate other pathologies. In this regard, allergy has been associated to metabolic disorders and with a higher risk of cardiovascular disease, but the underlying mechanisms remain incompletely understood. METHODS We used a murine model of allergy and atherosclerosis, different diets and sensitization methods, and cell-depleting strategies to ascertain the contribution of acute and late phase inflammation to dyslipidemia. Untargeted lipidomic analyses were applied to define the lipid fingerprint of allergic inflammation at different phases of allergic pathology. Expression of genes related to lipid metabolism was assessed in liver and adipose tissue at different times post-allergen challenge. Also, changes in serum triglycerides (TGs) were evaluated in a group of 59 patients ≥14 days after the onset of an allergic reaction. RESULTS We found that allergic inflammation induces a unique lipid signature that is characterized by increased serum TGs and changes in the expression of genes related to lipid metabolism in liver and adipose tissue. Alterations in blood TGs following an allergic reaction are independent of T-cell-driven late phase inflammation. On the contrary, the IgG-mediated alternative pathway of anaphylaxis is sufficient to induce a TG increase and a unique lipid profile. Lastly, we demonstrated an increase in serum TGs in 59 patients after undergoing an allergic reaction. CONCLUSION Overall, this study reveals that IgG-mediated allergic inflammation regulates lipid metabolism. | es_ES |
dc.description.sponsorship | R.J.-S.´s laboratory has received support from the Severo Ochoa Program (AEI/SEV-2017- 0712; Spain), FSE/FEDER through the Instituto de Salud Carlos III (ISCIII; CP20/00043; PI22/00236; Spain), The Nutricia Research Foundation (NRF-2021-13; The Netherlands), New Frontiers in Research Fund (NFRFE2019-00083; Canada) and SEAIC (BECA20A9; Spain). F.S.-M. reports grants from Ministerio de Ciencia e Innovación (MICIN; PID2020-120412RB-I00; Spain), and Comunidad de Madrid (INTEGRAMUNE, P2022/BMD7209; Spain). V.E. obtained support from the ISCIII (PI21/00158; Spain). N.F.-G. and I.R.-F. received a Formación de Profesorado Universitario grant (FPU16/03953 and FPU20/05176, respectively) from Ministerio de Universidades (Spain). N.F.-G. and L.M.-S. are supported by the INVESTIGO Program of the Comunidad deMadrid and Ministerio de Trabajo y Economía Social, Servicio Público de Empleo (SEPE), respectively, which is funded by “Plan de Recuperación, Transformacióny Resiliencia” and “NextGenerationEU” of the European Union (09- PIN1-00015.6/2022 and 2022-C23.I01.P03.S0020-0000031). R.C.-G. is supported by Ayudas para contratos Juan de la Ciervaformación 2021 (FJC2021-047282-I) from MICIN (Spain). C.L.-S. and E.N.-B. are supported by a Río Hortega (CM23/0019) and a Sara Borrell grant (CD23/00125), respectively, from ISCIII. P.M.is supported by MICIN-ISCIII-Fondo de Investigación Sanitaria (PI22/01759; PMPTA22/00090-BIOCARDIOTOX) and Comunidad de Madrid (P2022/BMD-7209-INTEGRAMUNE-CM; Spain) CNIC is a Severo Ochoa Center of Excellence (grant CEX2020-001041- Sfunded by MICIN/AEI/10.13039/501100011033). | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Wiley | es_ES |
dc.type.hasVersion | VoR | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.title | Allergic inflammation triggers dyslipidemia via IgG signalling. | es_ES |
dc.type | journal article | es_ES |
dc.rights.license | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.identifier.pubmedID | 38864116 | es_ES |
dc.identifier.doi | 10.1111/all.16187 | es_ES |
dc.contributor.funder | Ministerio de Ciencia e Innovación. Centro de Excelencia Severo Ochoa (España) | es_ES |
dc.contributor.funder | Comunidad de Madrid (España) | es_ES |
dc.contributor.funder | Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF) | es_ES |
dc.contributor.funder | Instituto de Salud Carlos III | es_ES |
dc.contributor.funder | Ministerio de Ciencia e Innovación (España) | es_ES |
dc.contributor.funder | Ministerio de Universidades (España) | es_ES |
dc.contributor.funder | Ministerio de Trabajo, Migraciones y Seguridad Social (España) | es_ES |
dc.description.peerreviewed | Sí | es_ES |
dc.identifier.e-issn | 1398-9995 | es_ES |
dc.relation.publisherversion | 10.1111/all.16187 | es_ES |
dc.identifier.journal | Allergy | es_ES |
dc.repisalud.orgCNIC | CNIC::Grupos de investigación::Comunicación Intercelular en la Respuesta Inflamatoria | es_ES |
dc.repisalud.orgCNIC | CNIC::Grupos de investigación::Laboratorio Traslacional para la Imagen y Terapia Cardiovascular | es_ES |
dc.repisalud.institucion | CNIC | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/EC/H2020/09-PIN1-00015.6/2022 | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/EC/H2020/2022-C23.I01.P03.S0020-0000031 | es_ES |
dc.rights.accessRights | open access | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/CP20/00043 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/PI22/00236 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/BECA20A9 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/PID2020-120412RB-I00 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/P2022/BMD7209 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/PI21/00158 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/FPU16/03953 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/FPU20/05176 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/FJC2021-047282-I | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/CM23/0019 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/CD23/00125 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/PI22/01759 | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/PMPTA22/00090-BIOCARDIOTOX | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/P2022/BMD-7209-INTEGRAMUNE-CM | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/ES/ MICIN/AEI/10.13039/501100011033/CEX2020-001041 | es_ES |