Inflammatory aging

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Anti aging (the English. Term inflammaging or inflammaging is also widespread in German-speaking) refers to the increased release of proinflammatory cytokines and related chronic diseases in the elderly.

description

The immunosenescence , aging of the immune system, is a part of aging. Inflammatory aging is characterized by a decline in the response of the adaptive immune system . The regression of the thymus begins with sexual maturity. This process is completed between the ages of 40 and 50. Thereafter, T-lymphocytes can no longer mature , which means that the immune system is dependent on the portfolio of T-lymphocytes formed up to that point. At a young age, the body has a high proportion of naive - that is, non-activated - T lymphocytes, a low proportion of memory cells and hardly any effector cells . In old age, on the other hand, the opposite is true: the effector cells dominate, the memory cells take second place and there are hardly any naive T lymphocytes left. This reversal results in changes in the cytokine secretion. Interleukin-2 and interleukin-4 are released significantly less than at a young age, while γ-interferon is formed to a greater extent . This in turn causes, among other things, a poorer maturation of the B lymphocytes and a reduced production of antibodies .

The term inflammaging was coined by the Italian immunologist Claudio Franceschi from the University of Bologna as a description for the generally accepted paradigm that aging is associated with the increased release of proinflammatory messenger substances . This condition of mild systemic and chronic (= subclinical) inflammation differs considerably from that of acute inflammation, which is characterized by five signs of inflammation .

Effects

Inflammatory aging has the effect, among other things, that the success of vaccinations is significantly lower in old age than in younger years.

In addition, inflammatory aging is seen as the cause of a number of age-associated diseases with inflammatory pathogenesis , such as arthritis , Alzheimer's , arteriosclerosis , osteoporosis and diabetes mellitus .

Inflammaging is also seen as a cause of the aging process itself. According to Franceschi's further hypothesis, inflammations are very helpful at a young age, where they considerably improve the chances of survival against pathogens, but according to the theory of antagonistic pleiotropy , they are more harmful to the organism in old age. This thesis is supported by the fact that the administration of sirolimus , an immunosuppressant , can significantly extend life expectancy in mice .

From an evolutionary point of view, the survival of an organism is important at least until the end of its reproductive phase. Most organisms (including early humans) died before they reached the end of the reproductive phase. The deleterious effects of inflammatory aging were thus very rare. A selection against this inflammation , which shortens the life span and which only occurs after the reproductive phase, was therefore not possible.

It is only for a short period of time - in terms of evolutionary history - that a large number of people have reached an age that exceeds 40 to 50 years. The immune system is not designed to reach old age, but must now be active for longer. This long period of activity leads to chronic inflammatory processes that slowly but inexorably cause damage to the organs - a phenomenon that is directly related to aging and to the typical age-related chronic diseases such as osteoporosis , sarcopenia , diabetes mellitus type 2 , Alzheimer's and atherosclerosis can result. Obviously, the progression of these diseases depends heavily on the genotype of the individual. There is a correlation that says that pro-inflammatory genotypes age earlier and, conversely, that a more controlled inflammatory status enables slower aging. Modern society means a significantly reduced pathogenic burden for the human organism - compared to the times when the immune system developed evolutionarily. An immune system adjusted to the current conditions would possibly increase life expectancy and suppress chronic age-related diseases.

Inflammatory aging is also seen as a possible cause of cancer . In centenarians, an increased gene expression was found that apparently better controls inflammatory processes.

further reading

Individual evidence

  1. ↑ G. Sergio: Exploring the complex relations between inflammation and aging (inflamm-aging): anti-inflamm-aging remodeling of inflammation, from robustness to frailty.  ( Page no longer available , search in web archives )  Info: The link was automatically marked as defective. Please check the link according to the instructions and then remove this notice. In: Inflammation Research 57, 2008, pp. 558-563. doi : 10.1007 / s00011-008-7243-2 PMID 19109735@1@ 2Template: Dead Link / resources.metapress.com  
  2. ^ A b F. Thalhammer: Vaccination in old age. (PDF file; 1.21 MB) In: Österreichische Ärztezeitung November 2008
  3. ^ A b B. Giunta, F. Fernandez, WV Nikolic, D. Obregon, E. Rrapo, T. Town, J. Tan: Inflammaging as a prodrome to Alzheimer's disease. In: Journal of neuroinflammation. Volume 5, 2008, p. 51, doi : 10.1186 / 1742-2094-5-51 , PMID 19014446 , PMC 2615427 (free full text) (review).
  4. ↑ a b c C. Franceschi et al .: Inflamm-aging. An evolutionary perspective on immunosenescence. In: Ann NY Acad Sci 908, 2000, pp. 244-254. PMID 10911963 (Review)
  5. ^ S. Vasto et al .: Inflammatory networks in aging, age-related diseases and longevity. In: Mech Aging Dev 128, 2007, pp. 83-91. PMID 17118425 (Review)
  6. ^ C. Franceschi et al.: Inflammaging and anti-inflammaging: a systemic perspective on aging and longevity emerged from studies in humans. In: Mech Aging Dev 128, 2007, pp. 92-105. PMID 17116321 (Review)
  7. ↑ G. Candore et al.: Biology of longevity: role of the innate immune system. In: Rejuvenation Res 9, 2006, pp. 143-148. PMID 16608411 (Review)
  8. ↑ C. Caruso et al .: Aging, longevity, inflammation, and cancer. In: Ann NY Acad Sci 1028, 2004, pp. 1-13. PMID 15915584 (Review)
  9. ^ DE Harrison et al.: Rapamycin fed late in life extends lifespan in genetically heterogeneous mice. In: Nature 460, 2009, pp. 392-395. PMID 19587680
  10. ^ C. Franceschi: Inflammaging as a major characteristic of old people: can it be prevented or cured? In: Nutr Rev 65, 2007, pp. S173-176. PMID 18240544
  11. ^ A b S. Vasto and C. Caruso: Immunity & Aging: a new journal looking at aging from an immunological point of view. In: Immun Aging 29, 2004, 1. PMID 15679921 ( Open Access )
  12. ↑ C. Franceschi and M. Bonafe: Centenarians as a model for healthy aging. In: Biochem Soc Trans 31, 2003, pp. 457-461. PMID 12653662 (Review)
  13. ↑ KS Krabbe et al .: Inflammatory mediators in the elderly. In: Exp Gerontol 39, 2004, pp. 687-699. PMID 15130663 (Review)
  14. ↑ D. Lio et al .: Inflammation, genetics, and longevity: further studies on the protective effects in men of IL-10 -1082 promoter SNP and its interaction with TNF-alpha -308 promoter SNP. In: Journal of medical genetics. Volume 40, Number 4, April 2003, pp. 296-299, PMID 12676903 , PMC 1735442 (free full text).
  15. ↑ G. Pawelec et al: T cells and aging. In: Front Biosci 7, 2002, pp. D1056-d1183. PMID 11991846 (Review)
  16. ↑ G. Candore et al: Immunological and Immunogenetic markers of successful and unsuccessful aging. In: Advances in Cell Aging and Gerontology 13, 2003, pp. 29-45.
  17. ↑ C. Caruso et al.: Looking for immunological risk genotypes. In: Ann NY Acad Sci 1019, 2004, pp. 141-146. PMID 15247007
  18. ^ G. Wick et al .: A Darwinian evolutionary concept of age-related diseases. In: Exp Gerontol 38, 2003, pp. 13-25.
  19. ^ L. Mariani et al .: Chronic antigenic stress, immunosenescence and human survivorship over the 3 last centuries: heuristic value of a mathematical model. In: Mech Aging Dev 124, 2003, pp. 453-458. PMID 12714253
  20. ^ S. Vasto et al .: Inflammation, aging and cancer. In: Mech Aging Dev 130, 2009, pp. 40-45. PMID 18671998

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