4. WHAT IS “INFLAMMAGING” / “INFLAMMATION AGING”?

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Inflammation aging describes the phenomenon that occurs in elderly people and results in chronic diseases thru significantly increased secretion of proinflammatory cytokines.

The immunosenescence, the aging of the immune system, is an epiphenomenon of aging. Inflammation aging is characterized by a decrease in the response of the adaptive immune system. The involution of the thymus starts at puberty and is completed between the age of 40 and 50. After this no maturation of T lymphocytes is possible, whereby the immune system depends on the portfolio of thitherto formed T-lymphocytes. At a young age, the body has a high proportion of naive – meaning not activated – T lymphocytes, a small amount of memory cells and only a few effector cells. In old age, however, it is exactly the reverse: It is dominated by the effector cells, memory cells are in second place and there are hardly any naive T lymphocytes present. This reversal results in changes in cytokine discharge. Interleukin-2 and interleukin-4 are significantly less distributed compared to young age, while γ-interferon is boosted. This in turn causes a lower maturation of B lymphocytes and a reduced production of antibodies [2].

The term “Inflammaging” was coined by the Italian immunologist Claudio Franceschi of the University of Bologna describing the generally accepted paradigm that aging is connected to an increased release of proinflammatory mediators. [3] [4] This state of slight systemic and chronic ( = subclinical) inflammation is very different from the acute inflammation that is characterized by five signs of inflammation.

Inflammation aging causes amongst others a significant lower success of vaccinations at a higher age than in younger years. [2]

In addition, inflammation aging is seen as a cause for a number of age-related diseases with inflammatory pathogenesis, such as arthritis, Alzheimer’s disease [3], arteriosclerosis, osteoporosis and diabetes mellitus. [5] [4]

Inflammaging is also seen as a cause of the aging process itself [6] Inflammation is – based on the hypothesis of Franceschi – at a young age very helpful, where it greatly enhances the chances of survival against pathogens, but becomes a problem later as according to the theory a lot of people reach an age, which goes beyond 40 to 50 years. The immune system is not designed to achieve a high age, but needs to be longer active. This long period of activity leads to chronic inflammatory processes that slowly – but inexorably – cause damage to the organs. This phenomenon is directly linked to aging and to the typical age-related chronic diseases such as osteoporosis, sarcopenia, type 2 diabetes, Alzheimer’s disease and atherosclerosis. [11] The progression of these disorders is obviously highly dependent on the genotype of the individual . [12] [13] There is a relationship, which states that pro-inflammatory genotypes age earlier and, conversely, that a more controlled inflammatory status allows a slower aging. [14] [15] [16] [17] Lifestyle and diet of modern, Western society lead to a significantly reduced pathogenic strain for the human body – compared to periods when the immune system developed evolutionarily. An immune system and gut microbiota [18] adapted to modern life would thus potentially increase the life expectancy and suppress chronic age-related diseases. [19] [11]

Inflammation aging is also seen as a possible cause of cancer. In centenarians a gene expression has been increasingly observed, which seems to better control inflammatory processes. [20]

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