This paper provide an interesting discussion of the interplay between oxidative stress, immune cell behavior, and raised inflammatory signaling in aging. Chronic inflammation is an important aspect of aging, disruptive of tissue and organ function throughout the body. Oxidative stress is the name given to a raised level of oxidative molecules present in and around cells, reacting with important proteins and other molecules to produce toxicity and disrupted function of cell components. This is also a noteworthy feature of aging. All aspects of aging interact with one another, and it is usually interesting to look into what is known of the details of any given interaction, as is done here.
The aging process can have multiple definitions depending on the perspective from which it is considered. From a biological point of view, the aging process may be defined as the progressive and general deterioration of the functions of the organism that leads to a lower ability to react to changes and preserve homeostasis adaptively. Homeostasis includes all processes that organisms use to actively maintain or adjust to appropriate conditions necessary for survival. Thus, although aging should not be considered a disease (it would be absurd to think of an illness that affects 100% of people), it is the main risk factor for the occurrence of chronic age-related diseases.
There are three physiological systems, the nervous, endocrine, and immune systems, in charge of maintaining body homeostasis. Moreover, these systems are in continuous communication, constituting a neuroimmunoendocrine system, which allows the preservation of homeostasis and, therefore, of health. With aging, there is a functional decline of these homeostatic systems and an impairment in the communication between them, which translates into a worse capacity to mount an adequate response to a variety of stressors. The decay of this capacity, which has also been referred to as decreased homeodynamic space or decreased homeostatic resilience, is what results in higher morbidity and mortality. Nevertheless, the age-related changes in these homeostatic systems are established at different rates in each subject, which translates into a different rate of aging or biological age of individuals with identical chronological age.
We believe that the rate at which these homeostatic systems decline relies on the establishment of a chronic oxidative and inflammatory stress situation. Thus, we describe how the oxidation inflammation theory of aging (oxi-inflamm-aging) is one of the most complete to describe how the process of aging occurs. Even though we are aware that the aging process is multifactorial, we propose mitochondrial reactive oxygen species (ROS) production as the first event involved in this process. In addition, we provide molecular mechanisms that link oxidation and inflammation and demonstrate how immune cells play an essential role in interconnecting both processes and, consequently, modulating the rate of aging. Accordingly, we show how the function and redox state of immune cells can be used as markers of the rate of aging of an individual allowing the prediction of lifespan. Moreover, to further confirm the role of immune cells in the aging process, we show, by modulating the redox and inflammatory state of immune cells and the production of oxidant and pro-inflammatory compounds by these cells, how different situations or conditions, such as the social environment, nutrition, and exercise, can have an impact on the lifespan of the organism.