Cytokine dysregulation is believed to play a key role in the remodeling of the immune system at older age, with evidence pointing to an inability to fine-control systemic inflammation, which seems to be a marker of unsuccessful aging. This reshaping of cytokine expression pattern, with a progressive tendency toward a pro-inflammatory phenotype has been called "inflamm-aging." Despite research there is no clear understanding about the causes of "inflamm-aging" that underpin most major age-related diseases, including atherosclerosis, diabetes, Alzheimer's disease, rheumatoid arthritis, cancer, and aging itself. While inflammation is part of the normal repair response for healing, and essential in keeping us safe from bacterial and viral infections and noxious environmental agents, not all inflammation is good. When inflammation becomes prolonged and persists, it can become damaging and destructive. Several common molecular pathways have been identified that are associated with both aging and low-grade inflammation. The age-related change in redox balance, the increase in age-related senescent cells, the senescence-associated secretory phenotype (SASP) and the decline in effective autophagy that can trigger the inflammasome, suggest that it may be possible to delay age-related diseases and aging itself by suppressing pro-inflammatory molecular mechanisms or improving the timely resolution of inflammation. Conversely there may be learning from molecular or genetic pathways from long-lived cohorts who exemplify good quality aging. Here, we will discuss some of the current ideas and highlight molecular pathways that appear to contribute to the immune imbalance and the cytokine dysregulation, which is associated with "inflammageing" or parainflammation. Evidence of these findings will be drawn from research in cardiovascular disease, cancer, neurological inflammation and rheumatoid arthritis.

/pdf/age-and-age-related-diseases-role-of-inflammation-triggers-cwvhq7tyyo.pdf

Age and Age-Related Diseases: Role of Inflammation Triggers and Cytokines.

Objective:Sepsis is an increasingly common and lethal medical condition that occurs in people of all ages. The influence of age on sepsis risk and outcome is incompletely understood. We sought to determine the independent effect of age on the incidence, severity, and outcome of adult sepsis.Design:L

The effect of age on the development and outcome of adult sepsis.

Proinflammatory cytokines, aging, and age-related diseases.

Inflammatory mediators in the elderly

It is now becoming apparent that the immune system undergoes age-associated alterations, which accumulate to produce a progressive deterioration in the ability to respond to infections and to develop immunity after vaccination, both of which are associated with a higher mortality rate in the elderly. Immunosenescence, defined as the changes in the immune system associated with age, has been gathering interest in the scientific and health-care sectors alike. The rise in its recognition is both pertinent and timely given the increasing average age and the corresponding failure to increase healthy life expectancy. This review attempts to highlight the age-dependent defects in the innate and adaptive immune systems. While discussing the mechanisms that contribute to immunosenescence, with emphasis on the extrinsic factors, particular attention will be focused on thymic involution. Finally, we illuminate potential therapies that could be employed to help us live a longer, fuller and healthier life.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-2567.2007.02555.x

Immunosenescence: emerging challenges for an ageing population

Altered cytokine production in the elderly

Dysregulation between TH1 and TH2 T cell subpopulations in the elderly.

The elderly are more prone to virus infections and neoplasias than are young adults. During a virus infection, interferon-α (IFN-α), proteins with antiviral, antiproliferative, and immunomodulatory properties, are transiently expressed. We here report that peripheral white blood cells from 16 subjects with a mean age of 72 years yielded less IFN when stimulated with a virus in vitro than those from 16 young adults with a mean age of 28 years. Monocytes are the main source of this IFN. However, yields of another monocyte product, interleukin-6 (IL-6), were greater in cells from the older subjects than from the young adults, so there is no general defect in monocytes from the former. Immunodeficiency in the elderly has been reported to be associated with a deficiency of zinc. When cultures of white blood cells from the elderly were supplemented with 15 μM zinc (the physiologic concentration), they produced IFN in amounts comparable to those from the younger subjects.

Zinc supplementation reconstitutes the production of interferon-alpha by leukocytes from elderly persons.

Overproduction of monokines by leukocytes after stimulation with lipopolysaccharide in the elderly.

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Altered cytokine production in the elderly

Dysregulation between TH1 and TH2 T cell subpopulations in the elderly.

Zinc supplementation reconstitutes the production of interferon-alpha by leukocytes from elderly persons.

Overproduction of monokines by leukocytes after stimulation with lipopolysaccharide in the elderly.