Abstract
Oxidative and inflammatory stresses are closely related processes, which contribute to age-associated impairments that affect the regulatory systems such as the immune system and its immunosenescence. Therefore, the aim of this work was to confirm whether an oxidative/inflammatory stress occurs in immune cells from adult mice with premature aging, similar to that shown in leukocytes from chronologically old animals, and if this results in immunosenescence. Several oxidants/antioxidants and inflammatory/anti-inflammatory cytokines were analyzed in peritoneal leukocytes from adult female CD1 mice in two models of premature aging—(a) prematurely aging mice (PAM) and (b) mice with the deletion of a single allele (hemi-zygotic: HZ) of the tyrosine hydroxylase (th) gene (TH-HZ), together with cells from chronologically old animals. Several immune function parameters were also studied in peritoneal phagocytes and lymphocytes. The same oxidants and antioxidants were also analyzed in spleen and thymus leukocytes. The results showed that the immune cells of PAM and TH-HZ mice presented lower values of antioxidant defenses and higher values of oxidants/pro-inflammatory cytokines than cells from corresponding controls, and similar to those in cells from old animals. Moreover, premature immunosenescence in peritoneal leukocytes from both PAM and TH-HZ mice was also observed. In conclusion, adult PAM and TH-HZ mice showed oxidative stress in their immune cells, which would explain their immunosenescence.
Highlights
Aging is characterized by a general and progressive deterioration of the physiological functions of the organism with a lessened capacity to maintain homeostasis and, an increase in morbidity and mortality
The aim of the present work was to confirm the establishment of oxi-inflamm-aging in peritoneal, spleen and thymus leukocytes from both adult prematurely aging mice (PAM) and Tyrosine Hydroxylase (TH)-HZ mice, which have been proposed as models of premature aging, and to determine whether their oxidative-inflammatory stress is similar to that observed in chronologically old mice
With the objective to analyze whether an inadequate immune response presented by cells from PAM and TH-HZ mice could be due to an altered cytokine network, we evaluated several pro-inflammatory (IL-1β, IL-6 and TNF-α) and anti-inflammatory IL-10 cytokine released by peritoneal leukocytes incubated in response to ConA and LPS
Summary
Aging is characterized by a general and progressive deterioration of the physiological functions of the organism with a lessened capacity to maintain homeostasis and, an increase in morbidity and mortality. The immune system, with advanced age, suffers numerous changes that affect the innate and acquired immune responses, which are called immunosenescence [2,3,4], and these have been related to the risk of suffering infections, autoimmune diseases and cancers [3,5,6,7]. In this context, several immune system parameters have been related to health and risk of mortality [5,8,9]. Several functional capacities of immune cells have been proposed as markers of the rate of aging of an individual and as predictors of life expectancy [10]
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