Sarcopenia is an age-related loss of skeletal muscle mass caused by many cellular mechanisms and also by lifestyle factors such as low daily physical activity. In addition, it has been shown that sarcopenia may be associated with inflammation and cognitive impairment in old age. Regular exercise is key in reducing inflammation and preventing sarcopenia and diseases related to cognitive impairment. The study was designed to assess the impact of exercise training on circulating apoptotic and inflammatory markers of sarcopenia in older adults. Eighty older adults aged 70.5 ± 5.8 years were randomized to the physically active group who participated in a 10-month Tai-Chi training session (TC, n = 40) and the control group who participated in health education sessions (HE, n = 40). Tai-Chi training caused a significant decrease in fat mass (FM) by 3.02 ± 3.99%, but an increase in appendicular skeletal muscle mass index (ASMI) by 1.76 ± 3.17% and gait speed by 9.07 ± 11.45%. Tai-Chi training elevated the plasma levels of C-reactive protein (CRP), tumor necrosis factor (TNFα), and tumor necrosis receptor factor II (TNFRII), and decreased caspases 8 and 9. Despite the increase in TNFα, apoptosis was not initiated, i.e., the cell-free DNA level did not change in the TC group. The study demonstrated that Tai-Chi training significantly reduced the symptoms of sarcopenia through the changes in body composition and physical performance, and improvements in cytokine-related mechanisms of apoptosis.

One of the latest theories on ageing focuses on immune response, and considers the activation of subclinical and chronic inflammation. The study was designed to explain whether anti-inflammatory diet and lifestyle exercise affect an inflammatory profile in the Polish elderly population. Sixty individuals (80.2 ± 7.9 years) were allocated to a low-grade inflammation (LGI n = 33) or high-grade inflammation (HGI n = 27) group, based on C-reactive protein concentration (<3 or ≥3 mg/L) as a conventional marker of systemic inflammation. Diet analysis focused on vitamins D, C, E, A, β-carotene, n-3 and n-6 PUFA using single 24-h dietary recall. LGI demonstrated a lower n-6/n-3 PUFA but higher vitamin D intake than HGI. Physical performance based on 6-min walk test (6MWT) classified the elderly as physically inactive, whereby LGI demonstrated a significantly higher gait speed (1.09 ± 0.26 m/s) than HGI (0.72 ± 0.28 m/s). Circulating interleukins IL-1β, IL-6, IL-13, TNFα and cfDNA demonstrated high concentrations in the elderly with low 6MWT, confirming an impairment of physical performance by persistent systemic inflammation. These findings reveal that increased intake of anti-inflammatory diet ingredients and physical activity sustained throughout life attenuate progression of inflammaging in the elderly and indicate potential therapeutic strategies to counteract pathophysiological effects of ageing.

The oxi-inflammatory response is part of the natural process mobilizing leukocytes and satellite cells that contribute to clearance and regeneration of damaged muscle tissue. In sports medicine, a number of post-injury recovery strategies, such as whole-body cryotherapy (WBC), are used to improve skeletal muscle regeneration often without scientific evidence of their benefits. The study was designed to assess the impact of WBC on circulating mediators of skeletal muscle regeneration. Twenty elite athletes were randomized to WBC group (3-min exposure to −120 °C, twice a day for 7 days) and control group. Blood samples were collected before the first WBC session and 1 day after the last cryotherapy exposure. WBC did not affect the indirect markers of muscle damage but significantly reduced the generation of reactive oxygen and nitrogen species (H₂O₂ and NO) as well as the concentrations of serum interleukin 1β (IL-1β) and C-reactive protein (CRP). The changes in circulating growth factors, hepatocyte growth factor (HGF), insulin-like growth factor (IGF-1), platelet-derived growth factor (PDGF^BB), vascular endothelial growth factor (VEGF), and brain-derived neurotrophic factor (BDNF), were also reduced by WBC exposure. The study demonstrated that WBC attenuates the cascade of injury–repair–regeneration of skeletal muscles whereby it may delay skeletal muscle regeneration.

Aging-related anemia contributes to frailty syndrome, cognitive decline and early mortality. The study aim was to evaluate inflammaging in relation to anemia as a prognostic indicator in affected older patients. The participants (73.0 ± 7.2 years) were allocated into anemic (n = 47) and non-anemic (n = 66) groups. The hematological variables RBC, MCV, MCH, RDW, iron and ferritin were significantly lower, whereas erythropoietin EPO and transferrin Tf tended toward higher values in the anemic group. Approx. 26% of individuals demonstrated transferrin saturation TfS < 20%, which clearly indicates age-related iron deficiency. The cut-off values for pro-inflammatory cytokine IL-1β, TNFα and hepcidin were 5.3 ng/mL, 97.7 ng/mL and 9.4 ng/mL, respectively. High IL-1β negatively affected Hb concentration (r_s = −0.581, p < 0.0001). Relatively high odds ratios were observed for IL-1β (OR = 72.374, 95%Cl 19.688–354.366) and peripheral blood mononuclear cells CD34 (OR = 3.264, 95%Cl 1.263–8.747) and CD38 (OR = 4.398, 95%Cl 1.701–11.906), which together indicates a higher probability of developing anemia. The results endorse the interplay between inflammatory status and iron metabolism and demonstrated a high usefulness of IL-1β in identification of the underlying causes of anemia, while CD34 and CD38 appeared useful in compensatory response assessment and, in the longer term, as part of a comprehensive approach to anemia monitoring in older adults.

Objective. The neurotrophin brain-derived neurotrophic factor (BDNF) affects poststroke functional outcome, neurogenesis, neuroprotection, and neuroplasticity. Its level is related to the diet and nutritional status, and more specifically, it is free fatty acids (FFAs) and eicosanoids that can have an impact on the BDNF level. The aim of this study was to analyze the potential impact of FFAs and eicosanoids on the BDNF level in stroke patients. Material and Methods. Seventy-three ischemic stroke patients were prospectively enrolled in the study. Laboratory tests were performed in all subjects, including the levels of FFAs, eicosanoids, and BDNF. FFAs and inflammatory metabolites were determined by gas chromatography and liquid chromatography, while BDNF was evaluated by the immune-enzymatic method (ELISA). Results. The plasma level of BDNF negatively correlated with C22:1n9 13 erucic acid, C18:3n3 linolenic acid (ALA), and lipoxin A4 15-epi-LxA4. A direct association was observed in relation to BDNF and C16:1 palmitoleic acid and C20:3n6 eicosatrienoic acid (dihomo-gamma-linolenic acid (DGLA)). Conclusions. Saturated fatty acids and omega-3 and omega-9 erucic acids can affect signaling in the BDNF synthesis resulting in the decrease in BDNF. There is a beneficial effect of DGLA on the BDNF level, while the effect of ALA on BDNF can be inhibitory. Specialized proresolving lipid mediators can play a role in the BDNF metabolism. BDNF can interact with inflammation as the risk factor in the cardiovascular disorders, including stroke.

Cytokines play an essential role in the control of tumor cell development and multiplication. However, the available literature provides ambiguous data on the involvement of these proteins in the formation and progression of glioblastoma (GBM). This study was designed to evaluate the inflammatory profile and to investigate its potential for the identification of molecular signatures specific to GBM. Fifty patients aged 66.0 ± 10.56 years with newly diagnosed high-grade gliomas and 40 healthy individuals aged 71.7 ± 4.9 years were included in the study. White blood cells were found to fall within the referential ranges and were significantly higher in GBM than in healthy controls. Among immune cells, neutrophils showed the greatest changes, resulting in elevated neutrophil-to-lymphocyte ratio (NLR). The neutrophil count inversely correlated with survival time expressed by Spearman’s coefficient r_s = −0.359 (p = 0.010). The optimal threshold values corresponded to 2.630 × 103/µL for NLR (the area under the ROC curve AUC = 0.831, specificity 90%, sensitivity 76%, the relative risk RR = 7.875, the confidence intervals 95%CI 3.333–20.148). The most considerable changes were recorded in pro-inflammatory cytokines interleukin IL-1β, IL-6, and IL-8, which were approx. 1.5–2-fold higher, whereas tumor necrosis factor α (TNFα) and high mobility group B1 (HMGB1) were lower in GBM than healthy control (p < 0.001). The results of the ROC, AUC, and RR analysis of IL-1β, IL-6, IL-8, and IL-10 indicate their high diagnostics potential for clinical prognosis. The highest average RR was observed for IL-6 (RR = 2.923) and IL-8 (RR = 3.151), which means there is an approx. three-fold higher probability of GBM development after exceeding the cut-off values of 19.83 pg/mL for IL-6 and 10.86 pg/mL for IL-8. The high values of AUC obtained for the models NLR + IL-1β (AUC = 0.907), NLR + IL-6 (AUC = 0.908), NLR + IL-8 (AUC = 0.896), and NLR + IL-10 (AUC = 0.887) prove excellent discrimination of GBM patients from healthy individuals and may represent GBM-specific molecular signatures.