The role of elastin peptides in modulating the immune response in aging and age-related diseases (original) (raw)

Next steps in mechanisms of inflammaging

Autophagy, 2020

Striking age-related changes occur in the human immune system, beginning in the sixth decade of life. Age is a non-modifiable, universal risk factor that results in the dysregulation of many cellular homeostatic processes. The decline in immune cell macroautophagy/autophagy and the increased generation of proinflammatory cytokines during agingfuels the development of diseases in the elderly. We reported that higher Th17 inflammation during aging was secondary to dysregulation in T cell autophagy. However, the mechanism underlying lower anti-CD3 and anti-CD28 activation-induced T cell autophagy during aging remain unknown. Our data fuel the speculation that dysregulation of the glutathione (GSH) system might cause the decline in T cell autophagy in aging, additionally provoked by reactive oxygen species signaling emanating from the mitochondria.

Interconnections between Inflammageing and Immunosenescence During Ageing

2021

Acute inflammation is a physiological response to injury or infection, with a cascade of steps that ultimately leads to recruitment of immune cells to clear invading pathogens and heal wounds. However, chronic inflammation arising from continued presence of the initial trigger, or dysfunction of signalling and/or effector pathways, is harmful to health. While successful ageing in older adults including centenarians is associated with low levels of inflammation, elevated inflammation increases the risk of poor health and death [1–3]. Hence inflammation has been described as one of seven pillars of ageing. Age-associated sterile, chronic, and low-grade inflammation is commonly termed inflammageing - it is not simply a consequence of increasing chronological age, but is also a marker of biological ageing, multimorbidity and mortality risk. While inflammageing was initially thought to be caused by “continuous antigenic load and stress”, reports from the last two decades describe a much ...

inflamation and its disease consequences.pdf

Inflammation is a self-defense event which is a result of any perturbation or interruption of body's homeostasis caused by biological, chemical, or physical agents as in infection and injury. This event leads to the initiation of inflammatory cascade which involves the production of pro-inflammatory mediators. In most cases this is an extremely important step in combating the pathogen, however when this inadvertently leads to a non-stop cascade not ready to slow down, the actual complications arise. The most dangerous aspect of this uncontrolled signaling is the birth of many diseases including cancer, atherosclerosis, arthritis, type 2 diabetes, sepsis etc. Although the basic players of all these diseases resulting from uncontrolled or chronic inflammation remain same, they differ in the propagation of the signal which in turn is dictated by the location and internal milieu of the organ it buds from. The review details the inflammatory pathway as well as the clinical implications diverging from it.

Editorial: The Physiology of Inflammation—The Final Common Pathway to Disease

Frontiers in Physiology, 2018

The 19 original and review articles included in the research topic "Physiology of Inflammation-the common pathway to disease" collectively convey an updated perspective on a variety of physiologic and pathologic conditions that trigger inflammation and how this response develops and progresses affecting tissue functions, either contributing to protect the organism or, instead, being a damaging process that disrupts homeostasis and drives most chronic diseases. While acute inflammation is usually a self-limited process, chronic inflammation, excluding that associated with autoimmune diseases, is characterized by a low-grade persistent inflammatory response that frequently is not clinically evident, but can be detected by the presence of increased levels of cytokines, chemokines, prostaglandins, nitric oxide, proteases, and other inflammatory mediators both at the tissue and plasma levels (Minihane et al., 2015). Accumulating evidence associates low grade inflammation with aging and the development and progression of most chronic diseases, from metabolic disturbances, like diabetes mellitus, obesity and the metabolic syndrome, to neurodegenerative, musculoskeletal, renal, cardiovascular diseases, and even behavioral diseases,

Molecular and cellular mechanisms of inflammation

Biochemistry (Moscow), 2016

Inflammation is one of the most fundamental and pronounced protective reactions of the organism. From ancient times to the present day, complex and diverse patterns of inflammation development and their role in various diseases have attracted attention of investigators. This issue of Biokhimiya/Biochemistry (Moscow) includes experimental studies and reviews dedicated to various aspects of this important and interesting problem.

Molecular Sciences The Link Between Inflammaging and Degenerative Joint Diseases

Aging is an inevitable process in the human body that is associated with a multitude of systemic and localized changes. All these conditions have a common pathogenic mechanism characterized by the presence of a low-grade proinflammatory status. Inflammaging refers to all the processes that contribute to the occurrence of various diseases associated with aging such as frailty, atherosclerosis, Alzheimer's disease, sarcopenia, type 2 diabetes, or osteoarthritis. Inflammaging is systemic, chronic, and asymptomatic. Osteoarthritis and many age-related degenerative joint diseases are correlated with aging mechanisms such as the presence of an inflammatory microenvironment and the impaired link between inflammasomes and autophagy. There is a close relationship between chondrocyte activity and local articular environment changes due to cell senescence, followed by secretion of inflammatory mediators. In addition, systemic inflammaging can lead to cartilage destruction, pain, disability, and an impaired quality of life. The purpose of this review is to summarize the main mechanisms implicated in inflammaging and the connection it has with degenerative joint diseases.

Inflammaging and Anti-Inflammaging: The Role of Cytokines in Extreme Longevity

Archivum immunologiae et therapiae experimentalis, 2015

Longevity and aging are two sides of the same coin, as they both derive from the interaction between genetic and environmental factors. Aging is a complex, dynamic biological process characterized by continuous remodeling. One of the most recent theories on aging focuses on immune response, and takes into consideration the activation of subclinical, chronic low-grade inflammation which occurs with aging, named "inflammaging". Long-lived people, especially centenarians, seem to cope with chronic subclinical inflammation through an anti-inflammatory response, called therefore "anti-inflammaging". In the present review, we have focused our attention on the contrast between inflammaging and anti-inflammaging systems, by evaluating the role of cytokines and their impact on extreme longevity. Cytokines are the expression of a network involving genes, polymorphisms and environment, and are involved both in inflammation and anti-inflammation. We have described the role o...