With the increase in life expectancy in humans, individuals are exposed longer to endogenous and environmental antigens which within the aging changes in the immune system and depletion of naive immune cells allows an activation of the innate immune system and the subsequent establishment of a low grade chronic inflammation state with increased expression of proinflammatory cytokines (tumor necrosis factor alpha, interleukin 6, heat shock protein 70). This inflammatory state referred as inflammaging in English spoken literature is characterized by an inflammatory origin of aging given by the activation of cellular systems responsible for gene promotion and suppression as the nuclear factor kappa B, sirtuins, forkhead box O and KLOTHO, who are directly or indirectly involved in cellular oxidative stress resistance mechanisms, apoptosis and nucleic acids transcriptional mistakes repair. The activation of these cellular systems is associated, in a molecular level, with the pathogenesis of several degenerative diseases in the elderly such as Alzheimer’s disease, late in life onset diabetes, cardiovascular diseases, functional impairment and disability. However, we are placed in a crossroad because we can’t establish if this inflammatory state observed in the aging process is responsible of the development of degenerative diseases or if the presence of these diseases is responsible of this inflammatory state of aging. Evidence in healthy centenarians who have preserved functional status has shown that there is a chronic inflammatory state present but that it is balanced by a higher expression of anti-inflammatory molecules.

Palabras clave: Aging inflammatory origin immunosenescence innate immunity nuclear factor kappa B tumor necrosis factor alpha interleukine-6.

2009-12-17   |   835 visitas   |   Evalua este artículo 0 valoraciones

Vol. 61 Núm.4. Julio-Agosto 2009 Pags. 327-336 Rev Invest Clin 2009; 61(4-ENGLISH)