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Investigation
Organ Transplant
Research projects
Content with Investigacion .
- Título: Desvelando la genómica de las bacterias anaerobias procedentes de bacteriemias
Referencia Proyecto: PID202-1127477OB-I00-MPY 302/22.
Entidad financiador: Agencia Estatal de Investigación.
Fechas de ejecución: 2023-2026
Financiación 108.900 €.
Investigadora principal: Sylvia Valdezate
- Título: Plataformas MALDI-TOF/CMI SENSITITRETM Personal Técnico Apoyo
Referencia: PTA2019-016623-I.
Entidad Financiadora: Agencia Estatal de Investigación.
Fechas ejecución 12/2020-11/2023
Investigadora principal: Sylvia Valdezate
- Título: Elementos genéticos móviles protagonistas en la evolución de los serotipos pandémicos M1 y M89 de Streptococcus pyogenes en el síndrome del shock tóxico y otras infecciones invasivas
Referencia: (MPY 377/18).
Entidad financiadora: Instituto de Salud Carlos III. Agencia Estatal de Investigación en Salud Intramural (AESI).
Fechas de ejecución: 11/2018-12/2022.
Financiación: 40.000 €.
Investigadoras principales: Pilar Villalón. Co-IP Sylvia Valdezate.
- Título: Plataformas genéticas y su influencia en la resistencia a co-trimoxazol, macrólidos y tetraciclina en Nocardia spp.
Referencia: MPY 1278/15
Entidad financiadora: Instituto de Salud Carlos III. Agencia Estatal de Investigación en Salud Intramural (AESI).
Fechas de ejecución: 2015-2017.
Financiación: 88.141,8 €.
Investigadora principal: Sylvia Valdezate
- Título: Filogenia y caracterización de mecanismos moleculares de resistencia en Nocardia spp.
Referencia: MPY 1446/11
Entidad financiadora: Instituto de Salud Carlos III. Fondo de Investigación Sanitaria (AES). ()
Fechas de ejecución: 04/2012-10/2015
Financiación: 115.457 €.
Investigadora principal: Sylvia Valdezate.
- Título: Iberian network of laboratories of biological alert. Accreditation of methods for detection highly pathogenic agents (IB-BIOALERTNET).
Entidad financiadora: COMISIÓN EUROPEA HOME/2012/ISEC/AG/CBRN/4000003810. (Instituto de Salud Carlos III (VISAVET, IVIA, INSA, INIAV))
Referencia: SAFI 1132/13-7.
Fecha de ejecución: 2013-2015.
Financiación: 699.175 €.
Tipo de participación: Miembro del equipo investigador.
- Título: EQUATOX Project Establishment of Quality Assurances for theDetection of Biological Toxins of potential Bioterrorism risk.
Entidad financiadora y convocatoria: Seven Framework Programme for Research FP7-SECURITY. (Robert Koch-Institut Berlin Alemania).
Referencia: SEC-2011.5.4-1.
Fechas de ejecución: 2012-2014.
Publications
Cryptococcus neoformans can form titan-like cells in vitro in response to multiple signals
Trevijano-Contador N, de Oliveira HC, García-Rodas R, Rossi SA, Llorente I, Zaballos Á, Janbon G, Ariño J, Zaragoza Ó. Cryptococcus neoformans can form titan-like cells in vitro in response to multiple signals. PLoS Pathog. 2018 May 18;14(5):e1007007. PMCID: PMC6454888.
PUBMED DOICell Wall Changes in Amphotericin B-Resistant Strains from Candida tropicalis and Relationship with the Immune Responses Elicited by the Host
5: Mesa-Arango AC, Rueda C, Román E, Quintin J, Terrón MC, Luque D, Netea MG, Pla J, Zaragoza O. Cell Wall Changes in Amphotericin B-Resistant Strains from Candida tropicalis and Relationship with the Immune Responses Elicited by the Host. Antimicrob Agents Chemother. 2016 Mar 25;60(4):2326-35. PMCID: PMC4808153.
PUBMED DOIThe production of reactive oxygen species is a universal action mechanism of Amphotericin B against pathogenic yeasts and contributes to the fungicidal effect of this drug
8: Mesa-Arango AC, Trevijano-Contador N, Román E, Sánchez-Fresneda R, Casas C, Herrero E, Argüelles JC, Pla J, Cuenca-Estrella M, Zaragoza O. The production of reactive oxygen species is a universal action mechanism of Amphotericin B against pathogenic yeasts and contributes to the fungicidal effect of this drug. Antimicrob Agents Chemother. 2014 Nov;58(11):6627-38. PMCID: PMC4249417.
PUBMED DOICapsule Growth in Cryptococcus neoformans Is Coordinated with Cell Cycle Progression
9: García-Rodas R, Cordero RJ, Trevijano-Contador N, Janbon G, Moyrand F, Casadevall A, Zaragoza O. Capsule growth in Cryptococcus neoformans is coordinated with cell cycle progression. mBio. 2014 Jun 17;5(3):e00945-14. PMCID: PMC4056547.
PUBMED DOIThe interaction between Candida krusei and murine macrophages results in multiple outcomes, including intracellular survival and escape from killing
12: García-Rodas R, González-Camacho F, Rodríguez-Tudela JL, Cuenca-Estrella M, Zaragoza O. The interaction between Candida krusei and murine macrophages results in multiple outcomes, including intracellular survival and escape from killing. Infect Immun. 2011 Jun;79(6):2136-44. PMCID: PMC3125833.
PUBMED DOIHuman IgM Inhibits the Formation of Titan-Like Cells in Cryptococcus neoformans
14: Trevijano-Contador N, Pianalto KM, Nichols CB, Zaragoza O, Alspaugh JA, Pirofski LA. Human IgM Inhibits the Formation of Titan-Like Cells in Cryptococcus neoformans. Infect Immun. 2020 Mar 23;88(4):e00046-20. PMCID: PMC7093138.
PUBMED DOIThe lymphocyte scavenger receptor CD5 plays a nonredundant role in fungal infection
15: Velasco-de-Andrés M, Català C, Casadó-Llombart S, Simões I, Zaragoza O, Carreras E, Lozano F. The lymphocyte scavenger receptor CD5 plays a nonredundant role in fungal infection. Cell Mol Immunol. 2020 Apr 24.
PUBMED DOIContent with Investigacion .
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Mónica Valiente Novillo
Técnico de laboratorio. Convocatoria empleo juvenial (PEJ-2021-TL_BMD-21100)
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Noelia Castrillo Garrido
Técnico de Laboratorio. Contratada de Proyecto PID2021-127477OB-I00 (AEI)
ORCID code: 0000-0003-1676-9693
List of staff
Additional Information
Induction of allograft tolerance remains a goal to be achieved in organ transplantation. Most therapeutic strategies focus on inhibition of the adaptive immune system, but recent data demonstrate that allogeneic recognition of myeloid cells initiates transplant rejection. Therapies targeting myeloid cells “in vivo” represent a potential target to induce immunological tolerance, but remain clinically unexplored.
Our laboratory uses a revolutionary nanoimmunotherapy of high-density lipoprotein (HDL) nanoparticles loaded with rapamycin (mTORi-HDL) that prevents epigenetic modifications associated with trained immunity, a recently discovered functional state of macrophages. Using an experimental mouse transplant model, our results demonstrate that the administration of this immunotherapy with mTORi-HDL prevents the immune response and promotes tolerance to the transplanted organ.
Our laboratory shows a multidisciplinary research approach articulated in three different objectives to evaluate the clinical relevance and therapeutic effects of immunotherapy in preparation for a clinical trial in organ transplantation. The general objectives will be aimed at confirming the identification of trained immunity as a biomarker and analytical value to predict the risk of rejection in transplant patients under three conditions: prolonged periods of ischemic reperfusion (IRI) (objective 1), allosensitization (objective 2) and infection (objective 3).
Induction of allograft tolerance remains a goal to be achieved in organ transplantation. Most therapeutic strategies focus on inhibition of the adaptive immune system, but recent data demonstrate that allogeneic recognition of myeloid cells initiates transplant rejection. Therapies targeting myeloid cells “in vivo” represent a potential target to induce immunological tolerance, but remain clinically unexplored.
Our laboratory uses a revolutionary nanoimmunotherapy of high-density lipoprotein (HDL) nanoparticles loaded with rapamycin (mTORi-HDL) that prevents epigenetic modifications associated with trained immunity, a recently discovered functional state of macrophages. Using an experimental mouse transplant model, our results demonstrate that the administration of this immunotherapy with mTORi-HDL prevents the immune response and promotes tolerance to the transplanted organ.
Our laboratory shows a multidisciplinary research approach articulated in three different objectives to evaluate the clinical relevance and therapeutic effects of immunotherapy in preparation for a clinical trial in organ transplantation. The general objectives will be aimed at confirming the identification of trained immunity as a biomarker and analytical value to predict the risk of rejection in transplant patients under three conditions: prolonged periods of ischemic reperfusion (IRI) (objective 1), allosensitization (objective 2) and infection (objective 3).