Neuroinflamación. la vía de la interleucina 1 (Neuroinflammation. the Interleukin-1 Pathway)

La neuroinflamación es una respuesta del sistema nervioso central (SNC) frente a una lesión, una infección o una enfermedad. Las células afectadas inducen la producción y liberación de citoquinas proinflamatorias con el fin de establecer una defensa eficaz en el huésped. Entre ellas, las citoquinas pertenecientes a la familia de la interleucina 1 (IL1) juegan un papel muy relevante en la respuesta inflamatoria de las células del sistema nervioso central, especialmente de la microglía, y en la regulación de la respuesta mediada por las células del sistema inmunitario. La activación de la vía mediada por la IL-1 pone en marcha un sistema de señalización intracelular que desencadena la expresión de genes proinflamatorios inducidos por diferentes factores de transcripción, entre ellos el factor nuclear κB (NF-κB) que juega un papel clave en los procesos inflamatorios. En este trabajo se resumen los aspectos más relevantes de la neuroinflamación y los procesos moleculares subyacentes a la vía de señalización mediada por IL-1 y NF-κB

Exercise Outcomes in Childhood Obesity-Related Inflammation and Oxidative Status

Childhood obesity is identified as one of the major public health issues to increase the risk for cardiometabolic diseases and related complications in adulthood. The literature has supported inflammation and oxidative stress as the primary underlying mechanisms involved in the pathogenesis of obesity-related diseases. Epidemiological evidence consistently shows the benefits of physical activity in the improvement of obesity-mediated inflammation and oxidative stress status. In this narrative mini-review, the available scientific evidence on the potential effects of exercise in alleviating these susceptibilities in childhood obesity will be assessed.S

Resistance training modulates reticulum endoplasmic stress, independent of oxidative and inflammatory responses, in elderly people

[EN] Aging is related to changes in the redox status, low-grade inflammation, and decreased endoplasmic reticulum unfolded protein response (UPR). Exercise has been shown to regulate the inflammatory response, balance redox homeostasis, and ameliorate the UPR. This work aimed to investigate the effects of resistance training on changes in the UPR, oxidative status, and inflammatory responses in peripheral blood mononuclear cells of elderly subjects. Thirty elderly subjects volunteered to participate in an 8-week resistance training program, and 11 youth subjects were included for basal assessments. Klotho, heat shock protein 60 (HSP60), oxidative marker expression (catalase, glutathione, lipid peroxidation, nuclear factor erythroid 2-related factor 2, protein carbonyls, reactive oxygen species, and superoxide dismutase 1 and 2), the IRE1 arm of UPR, and TLR4/TRAF6/pIRAK1 pathway activation were evaluated before and following training. No changes in the HSP60 and Klotho protein content, oxidative status markers, and TLR4/TRAF6/pIRAK1 pathway activation were found with exercise. However, an attenuation of the reduced pIRE1/IRE1 ratio was observed following training. Systems biology analysis showed that a low number of proteins (RPS27A, SYVN1, HSPA5, and XBP1) are associated with IRE1, where XBP1 and RPS27A are essential nodes according to the centrality analysis. Additionally, a gene ontology analysis confirms that endoplasmic reticulum stress is a key mechanism modulated by IRE1. These findings might partially support the modulatory effect of resistance training on the endoplasmic reticulum in the elderly.SI: Funding for this project was provided by the Department of Exercise Science and Health Promotion at Florida Atlantic University. B. Estébanez was supported by a fellowship from the Ministry of Science, Innovation and Universities, Government of Spain (FPU fellowship, reference FPU15/05051; EST18/0025

Efecto de un programa de ejercicio físico sobre la respuesta a proteínas mal plegadas en las células mononucleares de la sangre periférica de pacientes pediátricos con obesidad

La prevalencia de la obesidad infantil ha aumentado a nivel global de forma preocupante, especialmente por las consecuencias que se pueden manifestar en la edad adulta. Se ha demostrado que esta afección aumenta el estrés de retículo endoplásmico (ERE) y, por lo tanto, activa la respuesta a proteínas mal plegadas (UPR). El ejercicio físico es una de las principales propuestas para atajar este reto de salud pública y, específicamente, para resolver el ERE. Por consiguiente, el objetivo de este estudio fue la evaluación del efecto de un programa de entrenamiento combinado de fuerza y resistencia de 12 semanas sobre la UPR en células mononucleares de la sangre periférica (PBMC) de pacientes pediátricos obesos. Para ello, se distribuyeron aleatoriamente 12 niños obesos (9 – 11 años) en un grupo entrenado (GE, n = 8), que se sometió al protocolo de entrenamiento, y un grupo control (GC, n = 4), que mantuvo sus rutinas habituales. Se analizaron proteínas de la UPR (ATF4, ATF6 p50, BiP, CHOP, p-eIF2α, p-IRE1 y XBP1s) por Western Blot antes y después del periodo de entrenamiento. Los resultados demostraron que el entrenamiento atenuó el aumento en la fosforilación de eIF2α e IRE1 en comparación con el GC. Además, se observó un efecto tiempo x grupo en la expresión de CHOP tras el entrenamiento. Sin embargo, no se encontraron diferencias en la expresión de ATF4, ATF6 p50, BiP o XBP1 tras el periodo de entrenamiento. En conclusión, los resultados sugieren que el programa de entrenamiento promueve un alivio en el ERE de los pacientes pediátricos obesos. No obstante, se necesitan nuevas investigaciones para determinar la eficacia de programas de entrenamiento alternativos

Resistance Training Modulates Reticulum Endoplasmic Stress, Independent of Oxidative and Inflammatory Responses, in Elderly People

Aging is related to changes in the redox status, low-grade inflammation, and decreased endoplasmic reticulum unfolded protein response (UPR). Exercise has been shown to regulate the inflammatory response, balance redox homeostasis, and ameliorate the UPR. This work aimed to investigate the effects of resistance training on changes in the UPR, oxidative status, and inflammatory responses in peripheral blood mononuclear cells of elderly subjects. Thirty elderly subjects volunteered to participate in an 8-week resistance training program, and 11 youth subjects were included for basal assessments. Klotho, heat shock protein 60 (HSP60), oxidative marker expression (catalase, glutathione, lipid peroxidation, nuclear factor erythroid 2-related factor 2, protein carbonyls, reactive oxygen species, and superoxide dismutase 1 and 2), the IRE1 arm of UPR, and TLR4/TRAF6/pIRAK1 pathway activation were evaluated before and following training. No changes in the HSP60 and Klotho protein content, oxidative status markers, and TLR4/TRAF6/pIRAK1 pathway activation were found with exercise. However, an attenuation of the reduced pIRE1/IRE1 ratio was observed following training. Systems biology analysis showed that a low number of proteins (RPS27A, SYVN1, HSPA5, and XBP1) are associated with IRE1, where XBP1 and RPS27A are essential nodes according to the centrality analysis. Additionally, a gene ontology analysis confirms that endoplasmic reticulum stress is a key mechanism modulated by IRE1. These findings might partially support the modulatory effect of resistance training on the endoplasmic reticulum in the elderly