Innate immunity and inflammation in ageing: a key for understanding age-related diseases |
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Authors: | Email author" target="_blank">Federico?LicastroEmail author Giuseppina?Candore Domenico?Lio Elisa?Porcellini Giuseppina?Colonna-Romano Claudio?Franceschi Calogero?Caruso |
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Institution: | 1.Dipartimento di Patologia Sperimentale,Università di Bologna,Italy;2.Gruppo di Studio sull'Immunosenescenza,Dipartimento di Biopatologia e Metodologie Biomediche, Università di Palermo,Italy;3.Istituto Nazionale di Riposo e Cura per Anziani,Italy;4.Centro Interdipartimentale "L. Galvani",Università di Bologna,Italy |
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Abstract: | The process of maintaining life for the individual is a constant struggle to preserve his/her integrity. This can come at
a price when immunity is involved, namely systemic inflammation. Inflammation is not per se a negative phenomenon: it is the
response of the immune system to the invasion of viruses or bacteria and other pathogens. During evolution the human organism
was set to live 40 or 50 years; today, however, the immune system must remain active for much a longer time. This very long
activity leads to a chronic inflammation that slowly but inexorably damages one or several organs: this is a typical phenomenon
linked to ageing and it is considered the major risk factor for age-related chronic diseases. Alzheimer's disease, atherosclerosis,
diabetes and even sarcopenia and cancer, just to mention a few – have an important inflammatory component, though disease
progression seems also dependent on the genetic background of individuals. Emerging evidence suggests that pro-inflammatory
genotypes are related to unsuccessful ageing, and, reciprocally, controlling inflammatory status may allow a better chance
of successful ageing. In other words, age-related diseases are "the price we pay" for a life-long active immune system: this
system has also the potential to harm us later, as its fine tuning becomes compromised. Our immune system has evolved to control
pathogens, so pro-inflammatory responses are likely to be evolutionarily programmed to resist fatal infections with pathogens
aggressively. Thus, inflammatory genotypes are an important and necessary part of the normal host responses to pathogens in
early life, but the overproduction of inflammatory molecules might also cause immune-related inflammatory diseases and eventually
death later. Therefore, low responder genotypes involved in regulation of innate defence mechanisms, might better control
inflammatory responses and age-related disease development, resulting in an increased chance of long life survival in a "permissive"
environment with reduced pathogen load, medical care and increased quality of life. |
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