Innate immunity and inflammation in ageing: a key for understanding age-related diseases
Open accessAbstract
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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Chronic and low-grade inflammation can lead to tissue dysfunction and degeneration.
“Chronic and low-grade inflammation can lead to tissue dysfunction and degeneration.”
From Immunosenescence and Its Hallmarks: How to Oppose Aging Strategically? A Review of Potential Options for Therapeutic Intervention (2019) · cites this paper as [60]
In the course of aging, there is a reduction in the ability to endure consequences of antigenic, chemical, physical, and nutritional triggers of inflammation.
“In the course of aging, there is a reduction in the ability to endure consequences of antigenic, chemical, physical, and nutritional triggers of inflammation.”
From Immunosenescence and Its Hallmarks: How to Oppose Aging Strategically? A Review of Potential Options for Therapeutic Intervention (2019) · cites this paper as [60]
This leads to an increased production of pro-inflammatory cytokines and acute phase proteins.
“This leads to an increased production of pro-inflammatory cytokines and acute phase proteins (59, 60).”
From Immunosenescence and Its Hallmarks: How to Oppose Aging Strategically? A Review of Potential Options for Therapeutic Intervention (2019) · cites this paper as [60]
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Biology of Longevity: Role of the Innate Immune System
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- Authors
- Licastro, F., Candore, G., Lio, D., Porcellini, E., Colonna-Romano, G., Franceschi, C., & Caruso, C.
- Affiliations
- University of Bologna (IT)
- University of Palermo (IT)
- Istituto Nazionale di Riposo e Cura per Anziani (IT)
- Corresponding author
- Licastro, Federico
- Venue
- Immunity & Ageing
- Published
- 2005-05-18
- Volume
- 2
- Issue
- 1
- Pages
- 8-8
- ISSN
- 1742-4933 (ISSN-L)
- PMC
- PMC1166571
- OpenAlex
- W2115145729
- Cited by
- 453
- References
- 159
- Citations by year
- 2026: 2 · 2025: 9 · 2024: 13 · 2023: 9 · 2022: 15 · 2021: 33 · 2020: 24 · 2019: 34 · 2018: 23 · 2017: 30 · 2016: 23 · 2015: 24 · 2014: 33 · 2013: 24 · 2012: 29
- FWCI
- 6.71
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Immunity & Ageing (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Archivio istituzionale della ricerca (Alma Mater Studiorum Università di Bologna) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Nova Science Publishers (Nova Science Publishers, Inc.) (submittedVersion)
- Funders
- Ministero dell’Istruzione, dell’Università e della Ricerca
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- innate immunity, systemic inflammation, aging, age-related diseases, chronic inflammation, successful aging, evolutionary programming, Alzheimer's disease, atherosclerosis, diabetes mellitus, sarcopenia, cancer, immunosenescence
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