Bioquímica Médica y Biología Molecular e Inmunología (Datos de investigación)

URI permanente para esta colecciónhttps://hdl.handle.net/11441/161843

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    Evaluation of co-therapy with melatonin and methylprednisolone in Experimental Autoimmune Encephalomyelitis (EAE) [Dataset]
    (2024-08-01) Álvarez López, Ana Isabel; Álvarez Sánchez, Nuria; Cruz Chamorro, Iván; Santos Sánchez, Guillermo; Ponce España, Eduardo; Bejarano, Ignacio; Lardone, Patricia Judith; Carrillo Vico, Antonio; Universidad de Sevilla. Departamento de Bioquímica Médica y Biología Molecular e Inmunología; Carrillo Vico, Antonio; Álvarez López, Ana Isabel; Álvarez López, Ana Isabel; Fundación Progreso y Salud; Junta de Andalucía; Universidad de Sevilla. CTS160: NeuroInmunoEndocrinología Molecular
    The dataset includes the raw data from the clinical score and flow cytometry analyzes carried out in the work titled " Melatonin synergistically potentiates the effect of methylprednisolone on reducing neuroinflammation in the experimental autoimmune encephalomyelitis mouse model of multiple sclerosis". This study shows the protective synergistic effect of co-treatment with melatonin and methylprednisolone on reducing the severity of EAE by decreasing CD4+ lymphocytes, B cells, macrophages and dendritic cells in the CNS, as well as modulating the population of infiltrated T and B cells toward regulatory phenotypes to the detriment of pro-inflammatory effector functions. In addition, treatment with melatonin from the clinical onset of EAE improves the natural course of the EAE and the response to a subsequent treatment with methylprednisolone in a later relapse of the disease. Eight-week-old female C57BL/6N mice were immunized immunization with 100 μg of MOG35–55 (Cambridge Research Biochemicals, Cleveland) emulsified in CFA (Sigma) containing 50 μg of heat-killed Mycobacterium tuberculosis (H37Ra, ATCC 25177) by subcutaneous injection in both hind legs and two doses of intraperitoneal pertussis toxin (200 ng/day) (List Labs, California) on days 0 and 2 post-induction. Animals were randomly divided to receive melatonin at a concentration of 80 mg/kg and/or methylprednisolone at a concentration of 40 or 160 mg/kg in different treatment regimens. Mice were sacrificed at the peak of the disease (day 15 after induction) and after perfusion, the CNS was collected, homogenized and enzymatically dissociated with 1.87 mg/ml of collagenase IV (Worthington) and 0.25 mg/ml of DNase I (AppliChem) for 35 min at 37°C to obtain a suspension of single cells. Subsequently, a 37%:70% discontinous percoll gradient was carried out to isolate CNS-infiltrating mononuclear cells. To assess the profile of infiltrated immune cells in the CNS, cells were stained for the following antibodies against surface markers: CD45, CD4, CD8α, CD19, CD11b, CD11c, CD44, CD62L, B220, CD138, PD-1 (CD279), CTLA-4 (CD152), FAS (CD95), and CD25. To identify Treg and analyze intracellular production of TNF, IFN-γ and IL-10, after surface staining, cells were fixed and permeabilized using the The dataset includes the raw data from the clinical score and flow cytometry analyzes carried out in the work titled " Melatonin synergistically potentiates the effect of methylprednisolone on reducing neuroinflammation in the experimental autoimmune encephalomyelitis mouse model of multiple sclerosis". This study shows the protective synergistic effect of co-treatment with melatonin and methylprednisolone on reducing the severity of EAE by decreasing CD4+ lymphocytes, B cells, macrophages and dendritic cells in the CNS, as well as modulating the population of infiltrated T and B cells toward regulatory phenotypes to the detriment of pro-inflammatory effector functions. In addition, treatment with melatonin from the clinical onset of EAE improves the natural course of the EAE and the response to a subsequent treatment with methylprednisolone in a later relapse of the disease. Eight-week-old female C57BL/6N mice were immunized immunization with 100 μg of MOG35–55 (Cambridge Research Biochemicals, Cleveland) emulsified in CFA (Sigma) containing 50 μg of heat-killed Mycobacterium tuberculosis (H37Ra, ATCC 25177) by subcutaneous injection in both hind legs and two doses of intraperitoneal pertussis toxin (200 ng/day) (List Labs, California) on days 0 and 2 post-induction. Animals were randomly divided to receive melatonin at a concentration of 80 mg/kg and/or methylprednisolone at a concentration of 40 or 160 mg/kg in different treatment regimens. Mice were sacrificed at the peak of the disease (day 15 after induction) and after perfusion, the CNS was collected, homogenized and enzymatically dissociated with 1.87 mg/ml of collagenase IV (Worthington) and 0.25 mg/ml of DNase I (AppliChem) for 35 min at 37°C to obtain a suspension of single cells. Subsequently, a 37%:70% discontinous percoll gradient was carried out to isolate CNS-infiltrating mononuclear cells. To assess the profile of infiltrated immune cells in the CNS, cells were stained for the following antibodies against surface markers: CD45, CD4, CD8α, CD19, CD11b, CD11c, CD44, CD62L, B220, CD138, PD-1 (CD279), CTLA-4 (CD152), FAS (CD95), and CD25. To identify Treg and analyze intracellular production of TNF, IFN-γ and IL-10, after surface staining, cells were fixed and permeabilized using the
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    Acceso AbiertoDataset
    Anti-obesogenic effects of vegetable-derived protein hydrolysate [Dataset]
    (2024-08-01) Ponce España, Eduardo; Cruz Chamorro, Ivan; Santos Sánchez Guillermo; Álvarez López, Ana Isabel; Fernández-Santos, José María; Pedroche, Justo; Millán Linares, María del Carmen; Bejarano Hernando, Ignacio; Lardone, Patricia Judith; Carrillo Vico, Antonio; ; Universidad de Sevilla. Departamento de Bioquímica Médica y Biología Molecular e Inmunología; Carrillo Vico, Antonio; Ponce España, Eduardo; Ponce España, Eduardo; Junta de Andalucía; Ministerio de Ciencia e Innovación (MICIN). España; Universidad de Sevilla; Ministerio de Educación, Cultura y Deporte (MECD). España; Universidad de Sevilla. CTS160: NeuroInmunoEndocrinología Molecular
    Data was acquired for the study published in the article titled: Anti-obesogenic effect of lupin-derived protein hydrolysate through modulation of adiposopathy, insulin resistance and gut dysbiosis in a diet-induced obese mouse. This study examines the effects of a lupin protein hydrolysate (LPH) on obesity, adipose tissue dysfunction and gut dysbiosis in obese mice. LPH was characterized and protein concentration, ashes, moisture, fiber, fats, soluble sugars and phenol content were measured as described. Amino acid composition was determined using standard amino acid mix solution. The molecular weight profile was obtained by molecular exclusion chromatography. Eight-week-old male C57BL6/N mice were housed under standard conditions and mice were randomly assigned to three groups: mice fed a standard diet (SD), a high-fat diet (HFD) or an HFD and treated intragastrically with LPH (HFD+LPH) at a dose of 100mg/kg five days a week for 12 weeks. The SD and HFD groups were treated with vehicle under the same conditions as the HFD+LPH group. Food consumption and individual body weight were measured weekly. Animals were sacrificed with an intraperitoneal injection of sodium thiopental and blood was collected by cardiac puncture. Epidydimal adipose tissue (EpiWAT) was dissected, snap-frozen and stored at -80ºC until use or fixed in a 4% paraformaldehyde (PFA) solution. Stool was collected prior to euthanasia and stored at -80ºC. Serum biochemical profile was measured by chemoluminiscence in the Cobas Integra 400 (Roche Diagnostics, Indianapolis, IN, USA) at the Estación Biológica de Doñana (EBD-CSIC, Seville, Spain). Serum concentrations of leptin, adiponectin and insulin were quantified using enzyme-linked immunosorbent assays (ELISA) kits. Adipose tissue samples fixed in 4% PFA were dehydrated, embedded in paraffin blocks and sliced 4μm thick, stained with hematoxylin-eosin and cover mounted for posterior observation. Photomicrographs were obtained using Leica THUNDER microscope and Leica Application Suite X software. Adipocyte morphology and number of crown-like structures was blinded analyzed using ImageJ v1.53h public software. High throughput 16S rRNA gene amplicon analysis was performed using total DNA extracted from stool. 16S rRNA V3–V4 region was sequenced using MiSeq protocol and instruments. The raw sequences were processed using mothur.