Immunosenescence in Aging-Related Vascular Dysfunction

Abstract

The immunosenescence-related disproportion in T lymphocytes may have important consequences for endothelial dysfunction, which is a key event in vascular aging. The study was designed to assess the prognostic values of the inflammatory-immune profile to better predict and prevent vascular diseases associated with old age. Eighty individuals aged 70.9 ± 5.3 years were allocated to a low- (LGI) or high-grade inflammation (HGI) group based on CRP (< 3 or ≥ 3 mg/L) as a conventional risk marker of cardiovascular diseases. Significant changes in inflammatory and endothelium-specific variables IL-1β, IL-6, TNFα, oxLDL, H2O2, NO, 3-nitrotyrosine, and endothelial progenitor cells (OR 7.61, 95% CI 2.56–29.05, p < 0.0001), confirmed their interplay in vascular inflammation. The flow-cytometry analysis demonstrated a high disproportion in T lymphocytes CD4+ and CD8+ between LGI and HGI groups. CRP was < 3 mg/mL for the CD4/CD8 ratio within the reference values ≥ 1 or ≤ 2.5, unlike for the CD4/CD8 ratio < 1 and > 2.5. The odds ratios for the distribution of CD4+ (OR 5.98, 95% CI 0.001–0.008, p < 0.001), CD8+ (OR 0.23, 95% CI 0.08–0.59, p < 0.01), and CD8CD45RO+ T naïve cells (OR 0.27, 95% CI 0.097–0.695, p < 0.01) and CD4/CD8 (OR 5.69, 95% CI 2.07–17.32, p < 0.001) indicated a potential diagnostic value of T lymphocytes for clinical prognosis in aging-related vascular dysfunction.

Cytokine Profile in Development of Glioblastoma in Relation to Healthy Individuals

“…Numerous reports showed how different age-related pathologies, including cancer, revealed a common inflammatory status. In fact, inflammaging is characterized by the establishment of a systemic proinflammatory state with an increased level of wellknown pro-tumorigenic cytokines, such as IL-1β, IL-6, and TNFα [19,42]. In the elderly with high-grade inflammation (CRP ≥ 3 mg/L), elevated levels of pro-inflammatory cytokines IL-1β, IL-6, and TNFα were recorded when compared to older adults with low-grade inflammation (CRP < 3 mg/L) [19].…”

Exercise to Prevent Accelerated Vascular Aging in People Living With HIV

“…172 Senescent cells are stably viable and can influence neighboring cells by secreting proinflammatory cytokines and chemokines, angiogenic factors, metabolites, and growth factors (ie, senescence-associated secretory phenotype) that further contribute to inflammation, oxidative stress, and tissue dysfunction. 172,173 In the context of chronic HIV infection, it is thought that continual HIV antigen stimulation is associated with greater cell divisions, telomere erosion, and subsequently reduced proliferative capacity (ie, senescence) of T cells. 168 Emerging evidence indicates that senescent T cells and the accompanying senescence-associated secretory phenotype contribute to hypertension and vascular aging in people without HIV.…”

“…168 Emerging evidence indicates that senescent T cells and the accompanying senescence-associated secretory phenotype contribute to hypertension and vascular aging in people without HIV. [172][173][174][175][176] For example, the frequency of circulating senescent angiogenic CD4+ T cells, which are involved in endothelial regulation, is negatively related to FMD and systemic inflammation in people with hypertension. 177 Membrane microparticles shed from T cells can exacerbate endothelial dysfunction by reducing NO-mediated vasodilation via decreased endothelial nitric oxide synthase expression.…”

Cells in Atherosclerosis: Focus on Cellular Senescence from Basic Science to Clinical Practice

“…The adhesion of the enlarged senescence endothelial cells to the basal membrane is increased leading to impaired alignment to laminar shear stress, but resistance to denudation [45]. Aging results in the accumulation of these cells owing to the imbalance between endothelial senescent cell production and elimination, due to age-related immunosenescence [46]. Endothelial senescent cell accumulation leads to endothelial barrier dysfunction, increased levels of inflammatory cytokines (IL-1β, IL-6, IL-8), chemokines (chemokine ligand 11, MCP-1), growth factors, and ROS.…”