{"id":6441,"date":"2022-01-18T14:24:27","date_gmt":"2022-01-18T19:24:27","guid":{"rendered":"https:\/\/abudinen.com\/blog\/?p=6441"},"modified":"2022-01-18T21:07:17","modified_gmt":"2022-01-19T02:07:17","slug":"inmunidad-vs-cuarentenas","status":"publish","type":"post","link":"https:\/\/abudinen.com\/blog\/2022\/01\/18\/inmunidad-vs-cuarentenas\/","title":{"rendered":"Inmunidad vs cuarentenas"},"content":{"rendered":"\n

Habla la Biblia de cuarentenas? Son las cuarentenas y tapabocas necesarios o afectan la salud? Necesitamos vacunarnos? Es la fiebre enemiga o aliada? Este y otros temas en este art\u00edculo.<\/em><\/p>\n\n\n\n

Why fever can be your friend in times of illness<\/strong> Written by Maria Cohut, Ph.D.<\/a> on May 23, 2018 \u2014 Fact checked by Jasmin Collier https:\/\/www.medicalnewstoday.com\/articles\/321889<\/p>\n\n\n\n

Fevers are more than just a symptom of illness or infection, claim researchers; elevated body temperature sets in motion a series of mechanisms that regulate our immune system, they found.<\/p>\n\n\n\n

Fevers aren\u2019t always a bad sign; you may even have heard that mild fevers are a good indication that your immune system is doing its job. But fevers aren\u2019t just a byproduct of our immune response.<\/p>\n\n\n\n

In fact, it\u2019s the other way around: an elevated body temperature triggers cellular mechanisms that ensure the immune system takes appropriate action against the offending virus or bacteria.<\/p>\n\n\n\n

So say researchers hailing from two academic institutions in the United Kingdom: the University of Warwick in Coventry and the University of Manchester.<\/p>\n\n\n\n

Senior researchers Profs. David Rand and Mike White led teams of mathematicians and biologists to understand what happens at cellular level when fever takes hold.<\/p>\n\n\n\n

Their findings<\/a>, which have recently been published in PNAS<\/em>, reveal that higher body temperatures drive the activity of certain proteins that, in turn, switch genes responsible for the body\u2019s immune response on and off, as required.<\/p>\n\n\n\n

Temperature regulates NF-\u03baB dynamics and function through timing of A20 transcription<\/h2>\n\n\n\n

C. V. Harper, D. J. Woodcock, C. Lam, M. Garcia-Albornoz,  View ORCID Profile<\/a> A. Adamson, L. Ashall, W. Rowe, P. Downton, L. Schmidt, S. West, D. G. Spiller, D. A. Rand, and  View ORCID Profile<\/a> M. R. H. White<\/p>\n\n\n\n

 See all authors and affiliationsPNAS May 29, 2018 115 (22) E5243-E5249; first published May 14, 2018; https:\/\/doi.org\/10.1073\/pnas.1803609115<\/a><\/p>\n\n\n\n

  1. Edited by Ronald N. Germain, National Institutes of Health, Bethesda, MD, and approved April 27, 2018 (received for review March 7, 2018)<\/li><\/ol>\n\n\n\n

    Significance<\/strong> Inflammation is often accompanied by temperature change, but little is known about the role of temperature in the inflammatory response. We show that physiologically relevant temperature changes significantly perturb NF-\u03baB dynamics following TNF\u03b1 stimulation in single cells. Using experimentation informed by mathematical modeling, we found that these changes were mediated, at least in part, through the key feedback gene TNFAIP3\/A20. Curtailing A20 expression removed temperature sensitivity across the fever range (37 \u00b0C to 40 \u00b0C). Gene expression was generally unaffected between these temperatures, although a select set of NF-\u03baB\u2212regulated genes was up-regulated at early time points. These genes were predominantly involved in inflammation, signaling, and cell fate. The cellular response to inflammation may therefore be mechanistically and functionally regulated by temperature.<\/p>\n\n\n\n

    Abstract<\/strong> NF-\u03baB signaling plays a pivotal role in control of the inflammatory response. We investigated how the dynamics and function of NF-\u03baB were affected by temperature within the mammalian physiological range (34 \u00b0C to 40 \u00b0C). An increase in temperature led to an increase in NF-\u03baB nuclear\/cytoplasmic oscillation frequency following Tumor Necrosis Factor alpha (TNF\u03b1) stimulation. Mathematical modeling suggested that this temperature sensitivity might be due to an A20-dependent mechanism, and A20 silencing removed the sensitivity to increased temperature. The timing of the early response of a key set of NF-\u03baB target genes showed strong temperature dependence. The cytokine-induced expression of many (but not all) later genes was insensitive to temperature change (suggesting that they might be functionally temperature-compensated). Moreover, a set of temperature- and TNF\u03b1-regulated genes were implicated in NF-\u03baB cross-talk with key cell-fate\u2013controlling pathways. In conclusion, NF-\u03baB dynamics and target gene expression are modulated by temperature and can accurately transmit multidimensional information to control inflammation.<\/p>\n\n\n\n

    https:\/\/www.pnas.org\/content\/115\/22\/E5243<\/a><\/p>\n\n\n\n

    Vitamin C and Immune Function<\/strong> Anitra C. Carr and Silvia Maggini Additional article information<\/a> Abstract<\/strong> Vitamin C is an essential micronutrient for humans, with pleiotropic functions related to its ability to donate electrons. It is a potent antioxidant and a cofactor for a family of biosynthetic and gene regulatory enzymes. Vitamin C contributes to immune defense by supporting various cellular functions of both the innate and adaptive immune system. Vitamin C supports epithelial barrier function against pathogens and promotes the oxidant scavenging activity of the skin, thereby potentially protecting against environmental oxidative stress. Vitamin C accumulates in phagocytic cells, such as neutrophils, and can enhance chemotaxis, phagocytosis, generation of reactive oxygen species, and ultimately microbial killing. It is also needed for apoptosis and clearance of the spent neutrophils from sites of infection by macrophages, thereby decreasing necrosis\/NETosis and potential tissue damage. The role of vitamin C in lymphocytes is less clear, but it has been shown to enhance differentiation and proliferation of B- and T-cells, likely due to its gene regulating effects. Vitamin C deficiency results in impaired immunity and higher susceptibility to infections. In turn, infections significantly impact on vitamin C levels due to enhanced inflammation and metabolic requirements. Furthermore, supplementation with vitamin C appears to be able to both prevent and treat respiratory and systemic infections. Prophylactic prevention of infection requires dietary vitamin C intakes that provide at least adequate, if not saturating plasma levels (i.e., 100\u2013200 mg\/day), which optimize cell and tissue levels. In contrast, treatment of established infections requires significantly higher (gram) doses of the vitamin to compensate for the increased inflammatory response and metabolic demand.Keywords: <\/strong>ascorbate, ascorbic acid, immunity, immune system, neutrophil function, microbial killing, lymphocytes, infection, vitamin C https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC5707683\/<\/p>\n\n\n\n

    Does Regular Exercise Counter T Cell Immunosenescence Reducing the Risk of Developing Cancer and Promoting Successful Treatment of Malignancies?<\/strong> Oxid Med Cell Longev. 2017;2017:4234765. doi: 10.1155\/2017\/4234765. Epub 2017 Jul 2. PMID: 28751932; PMCID: PMC5511671.<\/p>\n\n\n\n

    Highlights:<\/p>\n\n\n\n