Добірка наукової літератури з теми "Innata"
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Статті в журналах з теми "Innata"
Bottino, Emanuel, and Andrés Alberto Ponce. "Respuesta inmunitaria innata pulmonar en la infección por Sars-Cov-2." Revista de la Facultad de Ciencias Médicas de Córdoba 79, no. 1 (March 7, 2022): 33–42. http://dx.doi.org/10.31053/1853.0605.v79.n1.30642.
Повний текст джерелаA. Hernández-Urzúa, Miguel, and Anabell Alvarado-Navarro. "Interleucinas e inmunidad innata." REVISTA BIOMÉDICA 12, no. 4 (October 1, 2001): 272–80. http://dx.doi.org/10.32776/revbiomed.v12i4.286.
Повний текст джерелаCruz-Hernández, Diego Sait, Saraí Remedios Sánchez-Aparicio, and Sergio Roberto Aguilar- Ruiz. "Respuesta inmunitaria innata antiviral." RA RIÓ GUENDARUYUBI 5, no. 15 (May 15, 2022): 44–60. http://dx.doi.org/10.53331/rar.v5i15.7472.
Повний текст джерелаEspinosa Rosales, Francisco Javier. "Inmunopatología de la infección por virus SARS-CoV-2." Acta Pediátrica de México 41, no. 4S1 (June 29, 2020): 42. http://dx.doi.org/10.18233/apm41no4s1pps42-s502070.
Повний текст джерелаMolina Ramírez, Nelson. "La moral: ¿innata o adquirida?" Revista Colombiana de Bioética 8, no. 1 (November 18, 2015): 89. http://dx.doi.org/10.18270/rcb.v8i1.785.
Повний текст джерелаMUTWIRI, G., V. GERDTS, M. LOPEZ, and L. A. BABIUK. "Immunidad innata y nuevos adyuvantes." Revue Scientifique et Technique de l'OIE 26, no. 1 (April 1, 2007): 147–56. http://dx.doi.org/10.20506/rst.26.1.1731.
Повний текст джерелаZepeda E, Guillermo, Carolina Gvirtzman K, Javiera Kreft V, Erika Inostroza V, and Patricia Díaz A. "Streptococcus pneumoniae e inmunidad innata." Revista chilena de enfermedades respiratorias 29, no. 2 (April 2013): 89–95. http://dx.doi.org/10.4067/s0717-73482013000200005.
Повний текст джерелаReyes Martín, E., M. I. Rodríguez Pastore, J. Monserrat Sanz, D. Díaz Martín, A. Prieto Martín, and M. Álvarez-Mon Soto. "Respuesta inmune innata o inespecífica." Medicine - Programa de Formación Médica Continuada Acreditado 10, no. 28 (March 2009): 1861–67. http://dx.doi.org/10.1016/s0304-5412(09)70597-9.
Повний текст джерелаReyes Martín, E., A. Prieto Martín, D. Díaz Martín, and M. Álvarez-Mon Soto. "Inmunidad innata e inmunidad adaptativa." Medicine - Programa de Formación Médica Continuada Acreditado 11, no. 28 (March 2013): 1760–67. http://dx.doi.org/10.1016/s0304-5412(13)70553-5.
Повний текст джерелаFurtado, Gil Dutra, and Leonardo Alves Farias. "UBRE CAPRINA Y INMUNIDAD INNATA: REVISIÓN BIBLIOGRÁFICA." ENVIRONMENTAL SMOKE 2, no. 3 (October 31, 2019): 17–27. http://dx.doi.org/10.32435/envsmoke.20192317-27.
Повний текст джерелаДисертації з теми "Innata"
Ruyra, Ripoll Àngels. "Liposomes as immunostimulant delivery nanosystems: characterization and application in zebrafish (Danio rerio) and rainbow trout (Oncorhyncus mykiss)." Doctoral thesis, Universitat Autònoma de Barcelona, 2014. http://hdl.handle.net/10803/285044.
Повний текст джерелаThe innate immune system is based on the non-specific recognition of conserved elements of the pathogenic metabolism. This recognition is primarily mediated by germ line encoded pattern-recognition receptors (PRRs), present in specialized cells of the innate immune system, that are able to recognize conserved molecular patterns associated to pathogens (PAMPs). This recognition will trigger different signaling pathways that will induce the transcription of pro-inflammatory cytokines and result in local inflammation. Therefore, the innate immune system can be modulated by administration of these PAMPs, simulating a natural pathogen–immune system encounter. The main hypothesis of this study was that, by encapsulation in the same nanoscaled delivery system, of several PAMPs, also called immunostimulants, we could improve their administration to different fish species. Also, that this delivery system would interact with the cells of the immune system generating its non-specific activation and improving the immune response against different infectious diseases. In this context, a novel immunostimulant delivery nanosystem based on liposomes encapsulating a bacterial lipopolysaccharide from Escherichia coli, and a synthetic analog of viral dsRNA, poly (I:C), has been developed. Our data shows that, these biocompatible liposomes were able to be endocytosed in vitro by zebrafish (Danio rerio) hepatocytes and rainbow trout (Oncorhynchus mykiss) macrophages as well as to regulate the expression of immune related genes. We have also developed a method for in vivo imaging of nano-sized liposomes in adult zebrafish, which allowed us to follow the dynamics and the target tissues of the liposomes administered either by intraperitoneal injection or immersion. The biodistribution results showed that the delivery system accumulated mainly in the spleen of zebrafish and in immune relevant cells, such as macrophages, from rainbow trout. Moreover, we showed that these liposomes, administrated by intraperitoneal injection and immersion, could effectively protect zebrafish from bacterial (Pseudomonas aeruginosa PAO1) and viral (spring viraemia of carp virus) infections. In conclusion, these findings suggest that the stimulation of the innate immune system with liposomes encapsulating a bacterial lipopolysaccharide and the synthetic analog of viral dsRNA, poly (I:C), could be a good strategy to achieve protection against bacterial and viral infections therefore potentially working as a non-specific prevention tool in fish.
Arranz, Trullén Javier. "Unveiling the multifaceted antimicrobial mechanism of action of human host defence RNases." Doctoral thesis, Universitat Autònoma de Barcelona, 2016. http://hdl.handle.net/10803/400666.
Повний текст джерелаThe present doctoral thesis is integrated into the large-scale study of the structure and function of human antimicrobial ribonucleases. These cationic and low molecular weight proteins are grouped into the ribonuclease A superfamily, considered one of the best characterized enzymes of the twentieth century. The RNase A superfamily is specific for vertebrates and has attracted remarkable interest due to the diversity of displayed biological properties; and represents an excellent example of a multifunctional protein´s family. Together with the main enzymatic activity we must highlight other biological properties such as the angiogenic, immunomodulatory and antimicrobial activities. The reported antimicrobial activity of distantly related family members in early vertebrates suggests that the family arouse with an ancestral function in host defence. Besides, the expression of several human RNases has been reported to be induced by infection. In particular, the RNases studied in this work, the human RNases 3, 6 and 7, are mainly expressed in eosinophils, monocytes and epithelial cells respectively. These proteins show a high cationicity due to the high proportion of basic residues and a remarkable antimicrobial activity against a wide range of human pathogens. Our research group has a consolidated experience in the study of the mechanism of action of human ribonucleases and the experimental work presented in this thesis is contributing to this overall research project. The main results achieved by the present PhD study are outlined below: - The characterization of the antimicrobial mechanism of RNase 6, both in bacteria cell cultures and using membrane models. Results highlight that the antimicrobial and cell agglutinating activities are mainly located at the N-terminus. - The resolution of the first three-dimensional structure of ribonuclease 6, obtained at 1.72 Å, which has set the structural basis for future functional studies. The kinetic characterization of RNase 6 mutant variants and the prediction of protein- substrate complexes have identified the enzyme nucleotide binding sites. - The study of the intracellular activity of ribonucleases 3, 6 and 7 and their derived Nterminal peptides against intracellular resident mycobacteria using a macrophage infected model. - The analysis of the anti-pathogenic mechanism of action of human antimicrobial proteins and peptides in mycobacterial infections and their applied therapies. - The comparative characterization of the antimicrobial mechanism of action of human RNases and their N-terminal derived peptides towards Candida albicans, as an eukaryote pathogen model. The results presented in this thesis will contribute to the understanding of the role of human RNases in the immune system and provide the structure- function basis to expand the initial project into the design of novel peptide mimetic therapeutics agents towards the eradication of resistant infectious diseases.
Escate, Chávez Oscar Rafael. "Efectos de la hipercolesterolemia sobre monocitos/macrófagos y la inmunidad innata." Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/400218.
Повний текст джерелаCardiovascular disease remains a leading cause of morbidity and mortality worldwide. The vast majority of cardiovascular events including coronary syndromes and stroke are cause by the rupture or erosion of atherosclerotic plaques in the arterial wall. Atherosclerosis is a complex dynamic disease characterized by lipid infiltration in arterial wall and a chronic inflammation response by cells of the innate immune system, mainly monocytes and macrophages. High levels of circulating low-density lipoproteins (LDL) are one of the major cardiovascular risk factors and subjects with Familial Hypercholesterolemia (FH), mainly caused by LDLR mutations affecting lipid metabolism, are at high risk of premature cardiovascular events. Currently it is well established the relevance of inflammation in the development of the atherosclerotic plaques, however, the effects of LDL on the phenotype and function of cells of the innate immunity, as monocyte and macrophage, are not fully understood. Further, the inflammatory response in macrophages of FH patients (from SAFEHEART Cohort) and its association with lifetime exposure to high LDLc levels has not been studied. In this thesis, we investigated the effect of atherogenic levels LDL on human monocyte and demonstrated that LDL facilitate monocyte differentiation into macrophage through a process that involves enhanced expression of cell-adhesion molecules and downregulation of apoptosis- effectors regulating anoikis in the early stage macrophages. This suggests a relevant role of LDL in the link between lipids, innate immunity and atherosclerosis. In patients FH, we demonstrated that LRP5, active lipid-internalizing receptor, is upregulated in innate immunity cells that have downregulated LDLR but retain the LDL internalization function. The reduced CD163 expression in these FH-macrophages also suggests less atheroprotection. We also show that monocyte-derived macrophages from FH patients treated according to guidelines have a sustained pro-inflammatory phenotype, characterized by an increased expression of chemokine receptors CCR3, CCR4, CXCR1 and a down-regulation of miR-505-3p, molecules related with inflammatory response. The effect is dependent on the age of the patient, suggesting a chronic inflammatory pattern in innate immunity cells that is related to epigenetic changes induced by lifetime exposure to high levels of LDL.
Suárez, Calvet Xavier. "Nous aspectes fisiopatogènics en la dermatomiositis." Doctoral thesis, Universitat Autònoma de Barcelona, 2015. http://hdl.handle.net/10803/302111.
Повний текст джерелаInflammatory myopathies are an heterogeneous group of neuromuscular diseases that are clinically characterized by the presence of muscle weakness that leads to disability. This group of diseases includes dermatomyositis (DM), polymyositis, inclusion body myositis and recently, necrotizing autoimmune myopathies have also been included. The study of the muscle biopsy, among other parameters, is necessary to obtain an accurate diagnosis. The muscle biopsy of these patients is characterized by the presence of inflammatory infiltrates that vary phenotypically and quantitatively in each entity. However, overexpression of the major histocompatibility complex class I (MHC-I) is shared by all these entities and it is believed that it has a pathogenic role. Until now, the etiology of DM is a matter of debate but there are two main hypotheses: The first hypothesis considers that the disease starts with an autoimmune attack against unknown antigens in the endothelium leading to the destruction of capillaries promoting, eventually, tissular hypoxia and muscle fiber atrophy. In fact, in the muscle biopsies of DM patients there is a characteristic reduction in the number of capillaries and perifascicular atrophy. The second hypothesis is based on the role of type I interferons (IFN-I). Experiments of gene expression analysis have demonstrated upregulation of multiple IFN-I-induced genes in DM. The origin of this IFN-I has been attributed to perimysial inflammatory infiltrates. To study the pathological mechanisms that occur specifically in the muscle fibers we isolated MHC-I positive muscle fibers using laser-microdissection from the muscle biopsies of these patients. This technology allowed us to exclude inflammatory infiltrates that could interfere with the results. The transcriptomic profile of the isolated fibers demonstrated a significant contribution of innate immunity, IFN-I and hypoxia specifically in DM. In particular, we observed the upregulation of RIG-I in DM, a receptor of the innate immunity that recognizes nucleic acids derived from virus to initiate an antiviral response and promoting IFN-I. Immunofluorescence studies demonstrated that RIG-I is overexpressed in MHC-I-expressing fibers in DM. In vitro studies using human myotubes showed the ability of RIG-I to induce the secretion of IFNβ – an IFN-I subtype – and as a consequence, induced the expression of MHC-I and RIG-I itself, suggesting a self sustained autoimmune mechanism in DM. These results prompted us to evaluate the relation between hypoxia and innate immunity. Hypoxia is mainly modulated by a key transcription factor named HIF1α that induces the expression of genes that contain specific sequences in its promoter. Our studies in silico and in vitro demonstrated that RIG-I is an HIF-inducible gene. From these studies, we concluded that hypoxia is a primary event in the pathogenic sequence of events in DM because the overexpression of RIG-Iwas able to induce its own activation promoting the expression of IFN-I-stimulated genes. In contrast, the expression of HIF1α was not modified by the stimulation of IFNs. Finally we evaluated the utility of RIG-I as a histological biomarker for DM. We studied 115 muscle biopsies using immunohistochemistry including diseases that may be confused clinically or histologically with DM. We demonstrated that RIG-I has a higher sensitivity than perifascicular atrophy for DM diagnosis (50% in DM vs 11 % in non-DM). Interestingly, 32% of patients with DM in whom perifascicular atrophy was not evident, showed expression of RIG-I at the perifascicular areas. We analyzed the reproducibility of perifascicular atrophy and RIG-I staining and we found that RIG-I has a higher reproducibility and therefore constitutes a more easily interpretable biomarker than perifascicular atrophy. We conclude that this thesis unifies both current hypotheses on DM pathogenesis and shows that hypoxia contributes to the pathology of DM by activating the RIG-I signaling pathway and consequently inducing IFN-I expression.
Martinez, Escala Maria Estela. "Estudi in vivo sobre la rellevància del sistema immune innat en la patogènia de la epidermòlisi ampul·lar adquirida." Doctoral thesis, Universitat Autònoma de Barcelona, 2016. http://hdl.handle.net/10803/400475.
Повний текст джерелаBackground: Epidermolysis bullosa acquisita (EBA) is a chronic autoimmune disorder characterized by the presence of circulating and tissue-bound autoantibodies against collagen VII (CVII), a protein localized at the dermal-epidermal basement membrane zone (BMZ). It is clinically manifested with tense blisters and erosions involving mucocutaneous tissues. Parts of the innate immune system have been demonstrated to be involved in tissue damage, particularly components of the complement system, antibodies’ receptors and neutrophils. Specifically, Rac2 protein is a GTPase involved in chemotaxis of neutrophils and reactive oxygen species synthesis through NADPH oxidase activation. Acute lung injury (ALI) is a syndrome induced by the immune response where the recruitment of neutrophils favors tissue damage evolving into an acute respiratory distress syndrome. In vivo studies performed in Rac2 knock-out (KO) mice and the pharmacological inhibition of Rac2 (NSC23766) in ALI have demonstrated a decrease in lung tissue injury. Objectives: To investigate the role of Rac2 protein in tissue injury developed in an in vivo experimental mouse model of EBA. Materials and Methods: EBA phenotype was induced by passive transfer of antibodies against a fragment of murine CVII (mCVIICr). Anti-mCVIICr IgG was obtained after rabbit immunization. IgG from immunized and non-immunized rabbits (used as negative controls) were purified and concentrated to inject mice. Two sets of experiments were performed with Rac2 KO mice (total n=10) and wild type mice as positive controls (n=3) by injecting rabbit anti-mCVIICr IgG. At the same time, a set of Rac2 KO mice (n=4) were injected with unspecific rabbit IgG as negative controls. A third set of experiments consisted in injecting rabbit anti-mCVIICr IgG in mice pre-treated with dexamethasone (n=3), dapsone (n=5) and NSC23766 (n=3), an experimental soluble inhibitor of Rac2. Clinical assessments, histology of skin biopsies, direct immunofluorescence (DIF), and enzyme-linked immunosorbent assays (ELISA) were performed. Results: WT mice injected with anti-mCVIICr IgG successfully developed the EBA phenotype, with significantly increased disease severity with higher doses of IgG (p=.05). In contrast, none of the Rac2 KO mice injected with anti-mCVIICr IgG developed the EBA phenotype, even though IgG and C3 were deposited at the BMZ, and circulating anti-mCVIICr IgG was detected by ELISA. Pre-treated WT mice with NSC23766, dexamethasone and dapsone developed disease initially with a trend of milder disease severity, yet we found no statistically difference in body surface area involvement at the end of the observation period when compared with positive controls (p=0.08). Conclusions: The fact that EBA lesions were not developed in Rac2 KO mice after the passive transfer of anti-mCVIICr IgG clearly suggests the involvement of Rac2 protein in EBA pathogenesis. Therefore, we propose Rac2 as a potential target for designing therapies specific for EBA and other IgG-mediated disease. However, an effective Rac2 inhibitor to be used as therapy is not yet available.
Tellechea, Recarte Mónica 1989. "Role of NFAT5 in macrophage polarisation." Doctoral thesis, Universitat Pompeu Fabra, 2017. http://hdl.handle.net/10803/585894.
Повний текст джерелаEls macròfags són cèl·lules del sistema immunitari innat que es troben en tots els òrgans. Als teixits, els macròfags actuen per mantenir la homeòstasi canviant ràpidament entre estats inflamatoris i antiinflamatoris per respondre eficientment a les pertorbacions que succeeixen en el seu entorn. Aquesta plasticitat funcional requereix l’expressió coordinada de gens que estan regulats per factors que encara no han estat completament caracteritzats. En aquest treball es volia estudiar la contribució del factor de transcripció NFAT5 com a regulador de les funcions dels macròfags en diferents condicions de polarització. Per això, varem generar macròfags clàssicament activats (M1) i activats de manera alternativa (M2), WT i deficients en NFAT5, i varem analitzar l’expressió de marcadors M1 i M2 a nivell de mRNA i a nivell de proteïna per tècniques de citometria de fluxe, de ELISA i de Western Blot. També es van estudiar funcions inflamatòries dels macròfags, com ara la capacitat per a eliminar bacteris intracel·lulars o la inducció de respostes Th1 en limfòcits T CD4. Finalment es varen dur a terme assajos in vivo amb tumors singènics de pulmó (Lewis lung carcinoma) i el carcinoma d’ovari (ID8) per a determinar si els macròfags deficients en NFAT5 tenen una menor capacitat antitumoral. En resum, els nostres resultats indiquen que NFAT5 contribueix preferentment en la inducció de funcions inflamatòries, com ara la inducció de respostes Th1 i la restricció de la progressió tumoral.
CANNAS, VALERIA. "Exploitation of Ebola Virus VP35 Protein to identify new drugs counteracting its type I IFN antagonism." Doctoral thesis, Università degli Studi di Cagliari, 2015. http://hdl.handle.net/11584/266615.
Повний текст джерелаARTUSO, IRENE. "DAMPs and PAMPs have distinct roles in neutrophil recruitment during cutaneous microbial infections." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2021. http://hdl.handle.net/10281/304783.
Повний текст джерелаIntradermal infections with C. albicans are eliminated by neutrophils recruited at the site of infection with an unknown mechanism. To dissect how neutrophils are recruited at the site of infection, we analyzed the involvement of PRR that recognize C. albicans (TLR4, TLR2, Dectin1 and Dectin2) as well as CARD9, activated downstream Dectins, and MyD88 that transduces the signal derived from TLRs. WT, PRR-deficient and CARD9-deficient mice did not show any defect in neutrophil recruitment after C. albicans intradermal injection. Diversely, MyD88-deficient mice do not recruit neutrophils after C. albicans skin infection. Since MyD88 is involved in IL-1 signaling, we tested the role of IL-1β and IL-1α, two vasoactive cytokines, in the initiation of inflammation and neutrophil recruitment. In vitro and in vivo studies revealed that both IL-1β and IL-1α were involved in this process. IL-1α is constitutively expressed in epithelial, endothelial and stromal cells and can be released through proteolytic cleavage or cell death, enhancing the production of CXCL1, a chemokine with neutrophil chemoattractant activity. We confirmed that CXCL1 production in vivo depends on IL-1α release. We concluded that PRRs were not involved in the initiation of the inflammatory process during primary Candida skin exposure. Diversely, the initiation of the inflammatory process during primary infection can be due to the unspecific release of alarmins (like IL-1α) by distressed cells, considered like DAMP, stimulating neutrophils recruitment at the site of infection. To investigate whether DAMPs and PAMPs could have distinct roles in neutrophil recruitment during microbial infections, we have used models of skin infection with different types of pathogens: a fungus, C. albicans, a Gram-positive bacterium Staphylococcus aureus and a Gram-negative, Pseudomonas aeruginosa.
Perea, Soriano Lídia. "Associació d'elements de la resposta immune innata a les infeccions bacterianes en malalties respiratòries cròniques." Doctoral thesis, Universitat Autònoma de Barcelona, 2020. http://hdl.handle.net/10803/671345.
Повний текст джерелаLas infecciones bacterianas respiratorias en pacientes con Enfermedad Pulmonar Obstructiva Crónica (EPOC) y con bronquiectasias son una de las principales causas de empeoramiento del pronóstico de estas enfermedades. A menudo estas infecciones causan episodios de agudización durante las cuales la sintomatología de los pacientes se agravia, llegando a requerir ingreso hospitalario para controlar la infección. Se conoce que estos pacientes sufren una inflamación pulmonar y sistémica que aparece durante la estabilidad clínica y se acentúa durante las agudizaciones. Además, se cree que el microambient inlamatorio pulmonar de estas enfermedades favorece la infección por determinados bacterias, como la Pseudomona aeruginosa y la Hemophilus influenzae, asociados con mayor severidad. Aun así, todavía se desconocen los mecanismos inmunológicos por los cuales hay pacientes que agudizan frecuentemente, denominados aguditzadors frecuentes (AF) y otros pacientes que no agudizan o lo hacen de manera poco frecuente (NF). Por estas razones, esta tesis pretende estudiar los diferentes elementos de la respuesta inmune innata local implicados en la defensa de las infecciones bacterianas, en dos enfermedades respiratorias de elevado impacto en la salud pública como son la MPOC y las bronquiectasias. El primer objetivo ha estado asociar los niveles pulmonares de Fatty-acid binding protein 4 (FABP4) en pacientes con MPOC con la presencia de infección respiratoria, severidad de la enfermedad y poblaciones celulares. El segundo objetivo se ha centrado en estudiar los niveles pulmonares de los péptidos antimicrobianos (Palmos) Lactoferrina, Lisozima, LL-37 y Secretory Leukocyte Protease Inhibitor (SLPI) como posibles marcadores pronóstico de futuras agudizaciones en pacientes con bronquiectasias. Por último, el tercer objetivo ha estado caracterizar diferentes perfiles inmunológicos de inflamación pulmonar en pacientes con bronquiectasias y asociar estos a los parámetros clínicos.
Respiratory bacterial infections in patients with Chronic Obstructive Pulmonary Disease (COPD) and patients with bronchiectasis are one of the main causes of worsening the prognosis. These infections can cause exacerbations, known as episodes of acute worsening of disease symptoms which sometimes require hospitalization to stabilize the infection. These patients suffer from systemic and pulmonary inflammation during clinical stability and are elevated during exacerbations. In addition, the pulmonary inflammatory microenvironment of these diseases is thought to promote infection by certain bacteria, such as Pseudomona aeruginosa and Hemophilus influenzae, which are associated with greater severity. However, the immunological mechanisms by which patients frequently exacerbate, called frequent exacerbators (AF), and other patients who do not exacerbate or infrequently (NF) are still unknown. For these reasons, this thesis aims to study the different elements of the local innate immune response involved in the defense of bacterial infections, in two respiratory diseases with high public health impact such as COPD and bronchiectasis. The first objective was to associate the pulmonary and systemic levels of Fatty-acid binding protein 4 (FABP4) in COPD patients with the presence of respiratory infection, disease severity, and cell populations. The second objective was to study the pulmonary and systemic levels of antimicrobial peptides (AMPs) Lactoferrin, Lysozyme, LL-37 and Secretory Leukocyte Protease Inhibitor (SLPI) as an outcome marker of future exacerbations in patients with bronchiectasis. Finally, the third objective was to characterize different profiles of pulmonary inflammation in patients with bronchiectasis.
Valenzuela, Díaz Rodrigo Hernán. "Efecto de un lipopeptido bacteriano y glucocorticoide en células de inmunidad innata: rol de p38." Tesis, Universidad de Chile, 2008. http://www.repositorio.uchile.cl/handle/2250/105269.
Повний текст джерелаComo parte del sistema inmune innato existe un grupo de receptores de reconocimiento de patrones (PRRs) capaces de detectar aquellos patrones moleculares asociados a patógenos (PAMPs). Entre estos PRRs, destacan los receptores de tipo Toll o TLRs. Dentro de esta familia de receptores, TLR2 reconoce PAMPs derivados de bacterias gram positivas, los que promueven la activación de la vía de señalización intracelular dependiente del adaptador molecular MyD88, que conduce a la activación de IKK y de las MAPKs, las que tienen un impacto fundamental sobre la expresión de citoquinas proinflamatorias. El estudio de los mecanismos fisiológicos de control de esta vía de señalización constituye un área de investigación relevante en inmunología. En este sentido, los glucocorticoides, anti-inflamatorios naturales, ejercen su efecto vía un receptor citoplasmático (GR) mediante procesos de trans-represión y de expresión de proteínas reguladoras. A pesar de esto, se desconoce su efecto sobre las vías de inducción de citoquinas pro-inflamatorias mediadas por TLR2, tal como la vía de p38. Basados en estos antecedentes, el objetivo general de esta memoria de título consistió en determinar la participación de p38 en la producción de TNF-α en células A549, inducida por un agonista de TLR2, Pam3Cys-Ser-Lys4, en presencia o ausencia de dexametasona. Los objetivos específicos se centraron en: 1) determinar la expresión de TNF-α, a nivel de transcrito y proteína, en células activadas con el agonista sintético Pam3Cys-Ser-Lys4, en presencia o ausencia de dexametasona 2) evaluar la fosforilación de la proteína quinasa p38 en células estimuladas con Pam3Cys-Ser-Lys4, en presencia o ausencia de dexametasona y 3) evaluar la contribución de la proteína quinasa p38 sobre la expresión de TNF-α en células estimuladas con Pam3Cys-Ser-Lys4, en presencia o ausencia de dexametasona. Los resultados obtenidos indican que la activación de TLR2 por Pam3Cys-Ser-Lys4 induce un aumento en la expresión de TNF-α, el que no es reprimido por dexametasona. Se observó una activación de la vía p38 inducida por Pam3Cys-Ser-Lys4, que está involucrada en la expresión de TNF-α. Por otro lado, constatamos que dexametasona ejerce su efecto anti-inflamatorio clásico mediante la expresión de moléculas reguladoras de la vía de p38, como la fosfatasa MKP-1. Sin embargo, no podemos descartar un efecto independiente de la expresión de genes regulados por el glucocorticoide. Además, observamos que dexametasona no actuaría en los eventos tempranos de señalización de la vía de TLR2, como lo constatamos con la fosforilación de p38. Estos datos demostrarían un mecanismo a través del cual los glucocorticoides regulan procesos inflamatorios inducidos por TLR2, con un impacto relevante en el desarrollo de la inmunidad innata y la inflamación
As part of innate immune system, it exists a group of pattern-recognition receptors (PRRs) capable of detecting those molecular pattern associated to pathogens (pathogenassociated molecular patterns; PAMPs). Among these PRRs, Toll-like receptors (TLRs) stand out. Inside this receptor family, TLR2 recognizes PAMPs derived from gram positive bacteria, thus promoting activation of MyD88-dependent intracellular pathway. It leads to IKK and MAPKs activation, which have a fundamental impact on the expression of proinflammatory cytokines. The study of the physiological control mechanisms of this pathway constitutes an area of relevant research in immunology. In this sense, glucocorticoids, natural anti-inflammatory molecules, exert its effect by a cytoplasmatic receptor (GR) by trans-repression mechanism and regulatory proteins expression. In spite of this, the effect of glucocorticoid on the TLR2-mediated pro-inflammatory cytokine pathway induction, specially on p38, is unknown. Based on these precedents, the general aim of this study was determining the role of p38 in TNF-α production in A549 cells induced with Pam3Cys-Ser-Lys4, a TLR2 agonist, in presence or absence of dexametasona. The specific objectives were centered to: 1) determine TNF-α expression, at messenger and protein level; 2) evaluate the p38 protein kinase phosphorylation and 3) evaluate the contribution of p38 protein kinase on TNF-α expression under the stimulation with Pam3Cys-Ser-Lys4, in presence or absence of dexamethasone. The results indicate that the activation of TLR2 by Pam3Cys-Ser-Lys4 induces an increase in TNF-α expression, which is not suppressed for dexamethasone. It also was observed an activation of p38 pathway induced by Pam3Cys-Ser-Lys4, that was involved in TNF-α expression. On the other hand, that dexametasona exert its classic anti-inflammatory effect by means of expression of regulatory molecules of the p38 pathway, as phosphatase MKP-1. Nevertheless, we can’t reject an independent effect from the expression of glucocorticoid regulated genes. Besides, dexamethasona wouldn’t work on early events of TLR2 signalling pathway, as we observed for p38 phosphorylation. This data would show a mechanism by which glucocorticoids regulates the TLR2- induced inflammatory processes, with a relevant impact in the processes involved in the development of the innate immunity and inflammation
Книги з теми "Innata"
Abdul-Wahid, Jibiril. Saboda innata. [Niamey]: Editions Gashingo, 2010.
Знайти повний текст джерелаhonoree, Churata Gamaliel 1894-1969, ed. Innata vocación del escritor Gamaliel Churata. Lima: Pakarina Ediciones, 2017.
Знайти повний текст джерелаJuan Ramón de la Portilla. El juego de su innata crueldad. Pinar del Río, Cuba: Ediciones Loynaz, 2011.
Знайти повний текст джерелаEzekowitz, R. Alan B., and Jules A. Hoffmann. Innate Immunity. New Jersey: Humana Press, 2002. http://dx.doi.org/10.1385/1592593208.
Повний текст джерелаEwbank, Jonathan, and Eric Vivier, eds. Innate Immunity. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-570-1.
Повний текст джерелаJonathan, Ewbank, and Vivier E, eds. Innate immunity. Totowa, N.J: Humana Press, 2008.
Знайти повний текст джерелаB, Ezekowitz R. Alan, and Hoffmann J. 1941-, eds. Innate immunity. Totowa, NJ: Humana Press, 2003.
Знайти повний текст джерелаInnaiah, N. Mānavavāda jarnalisṭ Innayya jarnī: Iṇḍiyā nuṇḍi Amerikā varaku.. = Maanavavaada journalist Innaiah journey. Haidarābād: Emeskō, 2013.
Знайти повний текст джерелаSun, Xiao-Hong, ed. Innate Lymphoid Cells. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-8387-9.
Повний текст джерелаAmarnath, Shoba, ed. Innate Lymphoid Cells. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0338-3.
Повний текст джерелаЧастини книг з теми "Innata"
Georgel, Philippe, Xin Du, Kasper Hoebe, and Bruce Beutler. "ENU Mutagenesis in Mice." In Innate Immunity, 1–16. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-570-1_1.
Повний текст джерелаVremec, David, and Ken Shortman. "The Isolation and Identification of Murine Dendritic Cell Populations from Lymphoid Tissues and Their Production in Culture." In Innate Immunity, 163–78. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-570-1_10.
Повний текст джерелаYokoyama, Wayne M., and Sungjin Kim. "Analysis of Individual Natural Killer Cell Responses." In Innate Immunity, 179–96. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-570-1_11.
Повний текст джерелаFerlazzo, Guido. "Isolation and Analysis of Human Natural Killer Cell Subsets." In Innate Immunity, 197–213. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-570-1_12.
Повний текст джерелаLegrand, Fanny, Gaetane Woerly, Virginie Driss, and Monique Capron. "Innate Immune Function of Eosinophils." In Innate Immunity, 215–40. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-570-1_13.
Повний текст джерелаArock, Michel, Alexandra Nours, Odile Malbec, and Marc Daëron. "Ex Vivo and In Vitro Primary Mast Cells." In Innate Immunity, 241–54. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-570-1_14.
Повний текст джерелаMartinez-Pomares, Luisa, and Siamon Gordon. "Murine Macrophages." In Innate Immunity, 255–72. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-570-1_15.
Повний текст джерелаHosmalin, Anne, Miriam Lichtner, and Stéphanie Louis. "Clinical Analysis of Dendritic Cell Subsets." In Innate Immunity, 273–90. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-570-1_16.
Повний текст джерелаAndré, Pascale, and Nicolas Anfossi. "Clinical Analysis of Human Natural Killer Cells." In Innate Immunity, 291–300. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-570-1_17.
Повний текст джерелаSwainson, Louise, Cedric Mongellaz, Oumeya Adjali, Rita Vicente, and Naomi Taylor. "Lentiviral Transduction of Immune Cells." In Innate Immunity, 301–20. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-570-1_18.
Повний текст джерелаТези доповідей конференцій з теми "Innata"
Lascano Aimacana, Diego Sebastian, Lourdes Sánchez Nacher, Vicent Fombuena Borrás, Sandra Rojas Lema, and Néstor Montañés Muñoz. "Flipped classroom aplicado a prácticas de laboratorio de la asignatura “Ampliación de Ciencia de Materiales”." In IN-RED 2020: VI Congreso de Innovación Educativa y Docencia en Red. Valencia: Universitat Politècnica de València, 2020. http://dx.doi.org/10.4995/inred2020.2020.11976.
Повний текст джерелаRayón Encinas, Emilio, and Juan López. "Proyecto docente innovador desarrollado en Grado en Ingeniería en Diseño Industrial y Desarrollo de Producto para la consecución de un Prototipo Funcional mediante trabajo en equipo." In In-Red 2016 - Congreso de Innovación Educativa y Docencia en Red de la Universitat Politècnica de València. Valencia: Universitat Politècnica València, 2016. http://dx.doi.org/10.4995/inred2016.2016.4402.
Повний текст джерелаCastiblanco Rodríguez, Catherine Lisveth, and Nubia Isabel Rojas Castillo. "MEDIADORES DE CONFLICTOS DESDE LA PRIMERA INFANCIA, UNA TRANSFORMACIÓN SOCIAL QUE SE SOSTIENE EN UNA EDUCACIÓN PRESENCIAL COMO VIRTUAL." In VI CONGRESO INVESTIGACIÓN, DESARROLLO E INNOVACIÓN DE LA UNIVERSIDAD INTERNACIONAL DE CIENCIA Y TECNOLOGÍA. Universidad Internacional de Ciencia y Tecnología, 2022. http://dx.doi.org/10.47300/978-9962-738-04-6-15.
Повний текст джерелаMendoza Fandiño, Gustavo Alfonso, Mónica del Socorro Duque Quintero, and Raúl Iván Mazo Velásquez. "Variantes en los receptores TLR2 y TLR4 asociados con susceptibilidad a mastitis: su papelen la respuesta inmunológica innata en vacas lecheras Holstein." In 6° Encuentro Nacional de Semilleros de Investigación Uniremington. Fondo Editorial Remington, 2017. http://dx.doi.org/10.22209/mensi.n6a48.
Повний текст джерелаRico Sesé/Rodriguez Calatayud, Javier/Nuria. "¿Podrán las máquinas diseñar ovejas eléctricas?" In IV Congreso Internacional de Investigación en Artes Visuales. ANIAV 2019. Imagen [N] Visible. Valencia: Universitat Politècnica de València, 2019. http://dx.doi.org/10.4995/aniav.2019.8933.
Повний текст джерелаHiguera Martínez, Óscar Iván, Liliana Fernández Samacá, and Andrea Catalina Alvarado Fajardo. "FOMENTO DE LA CREATIVIDAD EN ESTUDIANTES DE PRIMER AÑO DE INGENIERÍA A TRAVÉS DE PROYECTOS." In La formación de ingenieros: un compromiso para el desarrollo y la sostenibilidad. Asociación Colombiana de Facultades de Ingeniería - ACOFI, 2020. http://dx.doi.org/10.26507/ponencia.719.
Повний текст джерелаMahgoub, Yasmine, Rida Arif, and Susu Zughaier. "Pyocyanin pigment from Pseudomonas aeruginosa modulates innate immune defenses in macrophages." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0137.
Повний текст джерелаKamareddine, Layla, Hoda Najjar, Abeer Mohbeddin, Nawar Haj Ahmed, and Paula Watnick. "Between Immunity, Metabolism, and Development: A story of a Fly Gut!" In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0141.
Повний текст джерелаJaeger, Stefan, Su-Shing Chen, and Wen-Ran Zhang. "TCM in Innate Immunity: A YinYang-N-Element Hypothesis of the Innate Immunological System." In 2009 International Joint Conference on Bioinformatics, Systems Biology and Intelligent Computing. IEEE, 2009. http://dx.doi.org/10.1109/ijcbs.2009.91.
Повний текст джерелаJing, Jian, Elizabeth Davidson, Brent Pedersen, Daniel LaFlamme, Ivana V. Yang, and David A. Schwartz. "DNA Methylation And Innate Immune Tolerance." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1367.
Повний текст джерелаЗвіти організацій з теми "Innata"
Rivas Santiago, Bruno, César Enrique Rivas Santiago, Gretel Mendoza Almanza, and Yamilé López Hernández. Efecto de la contaminación del aire atmosférico en la respuesta inmune innata antimicobacteriana. Buenos Aires: siicsalud.com, September 2019. http://dx.doi.org/10.21840/siic/159560.
Повний текст джерелаAlexandrea (Lexi) Duscher, Alexandrea (Lexi) Duscher. Squid in Space: Symbiosis and Innate Immunity. Experiment, August 2017. http://dx.doi.org/10.18258/9855.
Повний текст джерелаLópez Trascasa, Margarita. El sistema del Complemento: un mecanismo innato de defensa. Sociedad Española de Bioquímica y Biología Molecular (SEBBM), April 2010. http://dx.doi.org/10.18567/sebbmdiv_rpc.2010.04.1.
Повний текст джерелаNelson, Corwin, Donald C. Beitz, Timothy A. Reinhardt, and John Lippolis. 1,25-Dihydroxyvitamin D3 Enhances Bovine Mammary Epithelial Innate Immune Responses. Ames (Iowa): Iowa State University, January 2010. http://dx.doi.org/10.31274/ans_air-180814-618.
Повний текст джерелаUmland, Timothy C. Cross-Species Virus-Host Protein-Protein Interactions Inhibiting Innate Immunity. Fort Belvoir, VA: Defense Technical Information Center, July 2016. http://dx.doi.org/10.21236/ad1012633.
Повний текст джерелаNakasone, Elizabeth S. Understanding the Effects of Cytotoxic Chemotherapeutics on the Innate Immune System. Fort Belvoir, VA: Defense Technical Information Center, March 2012. http://dx.doi.org/10.21236/ada570818.
Повний текст джерелаCamargo, Jesus A. Acosta, Dean Boyd, and John F. Patience. Differential Digestibility of Innate Versus Added Fat in the Diets of Growing Pigs. Ames (Iowa): Iowa State University, January 2015. http://dx.doi.org/10.31274/ans_air-180814-1353.
Повний текст джерелаCahill, Jesse. A targeted opsonization platform for programming innate immunity against rapidly evolving novel viruses. Office of Scientific and Technical Information (OSTI), September 2021. http://dx.doi.org/10.2172/1820519.
Повний текст джерелаModis, Yorgo. The Structural Basis of Pathogen Recognition by TLR Receptors of the Innate Immune System. Fort Belvoir, VA: Defense Technical Information Center, August 2008. http://dx.doi.org/10.21236/ada495581.
Повний текст джерелаWeilhammer, D. R. Investigating the role of innate immunity in viral encephalitis caused by Rift Valley fever virus. Office of Scientific and Technical Information (OSTI), October 2019. http://dx.doi.org/10.2172/1573140.
Повний текст джерела