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      Las citoquinas en el absceso hepático amebiano: un ejemplo de investigación inmunología en el ámbito clínico Translated title: Cytokines in amoebic liver abscess: an example of immunological research within the clinical scope

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          Abstract

          Resumen El propósito de esta revisión es resaltar la importancia de la investigación en el área de la inmunología y su aplicación en el ámbito clínico. En una primera parte se presentan los descubrimientos más importantes que ayudaron a dilucidar los principales procesos fisiológicos involucrados en las enfermedades y de esta manera ayudaron a redireccionar la investigación en el área de la inmunología. Seguido, se describe un ejemplo de investigación básica relacionada con el papel de las citocinas en el absceso hepático amebiano, mostrando el trabajo de varios grupos de investigación en el mundo, con el objetivo de entender la respuesta inmune contra el parásito. Lo anterior nos permite argumentar la relevancia que tiene la investigación inmunológica dentro del contexto clínico.

          Translated abstract

          Abstract The purpose of this review is to highlight the importance of research in immunology and its application in the clinical setting. The first part presents the most important discoveries that helped to elucidate the main physiological processes involved in the diseases and in this way helped to redirect research in immunology. Then, we describe an example of basic research related to the role of cytokines in the amoebic liver abscess, showing the work of several research groups in the world, with the aim of understanding the immune response against the parasite. This allows us to argue the relevance of immunological research within the clinical context.

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          Most cited references51

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          Interleukin (IL)-6 Directs the Differentiation of IL-4–producing CD4+ T Cells

          Interleukin (IL)-4 is the most potent factor that causes naive CD4+ T cells to differentiate to the T helper cell (Th) 2 phenotype, while IL-12 and interferon γ trigger the differentiation of Th1 cells. However, the source of the initial polarizing IL-4 remains unclear. Here, we show that IL-6, probably secreted by antigen-presenting cells, is able to polarize naive CD4+ T cells to effector Th2 cells by inducing the initial production of IL-4 in CD4+ T cells. These results show that the nature of the cytokine (IL-12 or IL-6), which is produced by antigen-presenting cells in response to a particular pathogen, is a key factor in determining the nature of the immune response.
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            Interleukin-6 (IL-6) as an anti-inflammatory cytokine: induction of circulating IL-1 receptor antagonist and soluble tumor necrosis factor receptor p55.

            The aim of this study was to investigate whether interleukin (IL)-6 induces the production of IL-1 and tumor necrosis factor (TNF) antagonists. Serial plasma samples were obtained from cancer patients participating in phase I and II trials of recombinant IL-6 administered as a 120-hour continuous intravenous (IV) infusion. Plasma IL-1 receptor antagonist (IL-1Ra) and soluble TNF receptor p55 (TNFsRp55) levels were measured by specific radioimmunoassays (RIAs). IL-1Ra levels increased rapidly, reaching peak values (9.6 +/- 1.7 ng/mL) within 2 to 4 hours of beginning treatment. Thereafter, levels promptly declined, reaching near baseline within 24 hours despite continuation of IL-6. TNFsRp55 plasma levels increased within 4 to 8 hours after initiating treatment and increased progressively throughout the duration of therapy. IL-1 beta and TNF-alpha plasma levels were below the detection limit in all samples tested. Peripheral blood mononuclear cells (PBMC) exposed to IL-6 produced only small amounts (1.56 +/- 0.3 ng/mL) of IL-1Ra, even in the presence of exogenous soluble IL-6 receptor (gp80). TNFsRp55 levels measured in the supernatants of IL-6-stimulated PBMC were below the detection limit of the assay. Macrophages generated by culturing monocytes in granulocyte-macrophage colony-stimulating factor (GM-CSF) were much more responsive to IL-6 than freshly isolated unfractionated or adherent PBMC and synthesized almost as much IL-1Ra when stimulated with IL-6 as with endotoxin. These results suggest that the antinflammatory properties of IL-6 may be due; in part, to the induction of IL-1Ra synthesis and the release of soluble TNF receptors. Our findings also suggest that tissue macrophages may be an important source of IL-6-induced IL-1Ra.
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              Defective inflammatory response in interleukin 6-deficient mice

              Systemic and localized inflammation elicit a number of host responses which include fever, cachexia, hypoglycemia, and major changes in the concentration of liver plasma proteins. Interleukin 6 (IL-6) is considered an important mediator of the inflammatory response, together with IL-1 and tumor necrosis factor alpha (TNF-alpha). The purpose of this study was to unequivocally determine the role of IL-6 in these phenomena making use of IL-6-deficient mice that we have recently generated by gene targeting. We report here that in the absence of IL- 6, mice are unable to mount a normal inflammatory response to localized tissue damage generated by turpentine injection. The induction of acute phase proteins is dramatically reduced, mice do not lose body weight and only suffer from mild anorexia and hypoglycemia. In contrast, when systemic inflammation is elicited through the injection of bacterial lipopolysaccharide (LPS), these parameters are altered to the same extent both in wild-type and IL-6-deficient mice, demonstrating that under these conditions IL-6 function is dispensable. Moreover, we show that LPS-treated IL-6-deficient mice produce three times more TNF-alpha than wild-type controls, suggesting that increased TNF-alpha production might be one of the compensatory mechanisms through which a normal response to LPS is achieved in the absence of IL-6. We also show that corticosterone is normally induced in IL-6-deficient mice, demonstrating that IL-6 is not required for the activation of the hypothalamic-pituitary-adrenal axis. Our results reinforce the idea that different patterns of cytokines are involved in systemic and localized tissue damage, and identify IL-6 as an essential mediator of the inflammatory response to localized inflammation.
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                Author and article information

                Journal
                nova
                Nova
                Nova
                Universidad Colegio Mayor de Cundinamarca (Bogotá, Distrito Capital, Colombia )
                1794-2470
                June 2019
                : 17
                : 31
                : 97-108
                Affiliations
                [1] Bogotá Bogotá orgnameUniversidad Colegio Mayor de Cundinamarca orgdiv1Departamento de Bacteriología Colombia
                [2] Bogotá D.C. orgnameSecretaría de Educación del Distrito Colombia
                Article
                S1794-24702019000100097 S1794-2470(19)01703100097
                13880f1b-56e3-485e-8f3c-c596fe5663e2

                This work is licensed under a Creative Commons Attribution 4.0 International License.

                History
                : 29 December 2018
                : 15 October 2018
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 59, Pages: 12
                Product

                SciELO Colombia

                Categories
                Artículo de revisión

                inmunología,absceso hepático amebiano,medicina clínica,inmunology,citoquinas,citokines,clinical medicinal,amoebic liver abscess

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