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AGING AND INFLAMMATION Dra. Liseti Solano Rodríguez y M.Sc. Junedy Marcano. Instituto de Investigaciones en Nutrición. Universidad de Carabobo. Venezuela. Correo: [email protected] y [email protected] The increase of life expectancy along with decrease in birth rate has originated an explosive growth of the number and proportion of senior adults. This epidemiological fact emphasizes the importance of knowing the differences between aging successfully and not so successfully to be able to make a contribution to this process in order to lower medical and other inherent social costs. One very important fact in aging is the coexistence of alterations of the immune response, humoral and cellular, known as immunosenescence; which contributes to increased susceptibility to infections, cancer and other auto immune ailments. Fortunately these alterations are counterbalanced by body adaptation which occurs with time and thus allows observation of those adults who manage to live for more than hundred years. Aging is a postmaturational event associated to an increased predisposition to becoming sick and dying, for example a senior adult compared to a person less than 44 years has forty three times the probability of getting cancer, eighty nine times to suffer from pneumonia, ninety two times cardiac diseases and hundred times the possibility of being a victim to ACVs and chronic pulmonary sicknesses. The susceptibility to and survival from these sicknesses depends greatly on an optimal functioning of the immune system. During aging, there is a process of activation of a systemic, chronic, controlled, low intensity and asymptomatic inflammatory response; changes that are common to most of aging sicknesses. The inflammatory process is an extremely complex response to different internal and ambiental stimuli in which the principal participants are the pro inflammatory cytokines. Inflammation generates oxygen reactive species which not only causes oxidative damage but also amplifies the response of cytokines and forms a vicious cycle generating a chronic pro inflammatory state in which a lesion is created,and tisular reparation follows and damage accumulates over time, thus promoting aging and chronic associated ailments such as osteoporosis, sarcopenia, diabetes type 2, Alzheimer, and atherosclerosis. Various authors suggest that this phenomenon is the consequence of an evolutive genetic programming in which the pro inflammatory immune response is activated continuously defending and maintaining life against internal and external aggressions especially in the first few years. Due to the increase in the span of life, chronic inflammation occurs and tissue damage appears. To take into account genetic aspects related to better or worse aging an immunological risk phenotype (IRP) indicator is used. This indicator uses immune response parameters and maybe associated to the incapacity to control systemic inflammation as has been shown in a study of healthy Danish elderly in which it was observed an association between rate of mortality of all causes with slight elevation of tumoral necrosis factor (TNF-α) and interleukina-6 (IL-6), independently from each other and other assessed factors. To date, the factors responsible for the individual susceptibility are not known but they are under intense research. It is believed that this susceptibility may be multi factorial including genetic and ambiental interactions in the control of various parameters such as cytokine concentration, hormone concentration and the function of hormonal receptors, anti oxidation defense and reparation of DNA, function of proteosoma, control of apoptosis, state of histone acetilation, level of cells such as NK cells, or suppressor cells such as CD4+ CD25+ and positive and negative molecular co-stimulators over T cells. It is important that evaluate how much of these changes can be attributed to the immunogenetic baggage and how much on the natural history of the individual (effect of elevated anti genetic charges as it happens in chronic infections). Recent data indicate that some polymorphisms (IL-6-174 C/G) related to the production of interleukina-6 are predictive to the mortality of elderly people due to infarct of the myocardium or unstable angina and that there is a significant increase in the antiinflammatory genotype (IL-10 -1082GG/TNF-α-308GG) in people over hundred in comparison to control groups. This suggests that those persons with a genotype capable of controlling inflammatory states will age better whereas those with pro inflammatory genotypes will not age well. Bibliografía: Pawelec G., Ouyanga Q, Colonna-Romanob G, Candoreb G, Liob D and Carusob C.. Is human immunosenescence clinically relevant? Looking for “immunological risk phenotypes”. Trends in Immunology: 23(7):330-332, 2002. H. Bruunsgaard. Aging and proinflammatory cytokines. Curr Opin Hematol 8:131136. 2001. Stephen K. Butcher and Janet M. Lord. Stress responses and innate immunity: aging as a contributory factor. Aging Cell. 151–160. 2004 Vasto S, Malavolta M and Pawelec G: Age and immunity. Immunity & Ageing, 3:2. 2006 Arlt, W. and Hewison, M. Hormones and immune function: implications of aging. Aging Cell. 3(4): 209–216, 2004 Giunta S, Is inflammaging an auto[innate]immunity subclinical syndrome?Immunity & Ageing 2006, 3:12. Panda A, Arjona A, Sapey E, Bai F, Fikrig E, Montgomery RR, Lord JM, Shaw AC. Human innate immunosenescence: causes and consequences for immunity in old age. Trends Immunol. 30(7):325-33. 2009.