Endothelial progenitor cells (EPCs) have been suggested to constitute a restoration index of the disturbed endothelium in ICU patients. Neuromuscular electric stimulation (NMES) is increasingly employed in ICU to prevent comorbidities such as ICU-acquired weakness, which is related to endothelial dysfunction. The role of NMES to mobilize EPCs has not been investigated yet. The purpose of this study was to explore the NMES-induced effects on mobilization of EPCs in septic ICU patients. Thirty-two septic mechanically ventilated patients (mean ± SD, age 58 ± 14 years) were randomized to one of the two 30-min NMES protocols of different characteristics: a high-frequency (75 Hz, 6 s on–21 s off) or a medium-frequency (45 Hz, 5 s on–12 s off) protocol both applied at maximally tolerated intensity. Blood was sampled before and immediately after the NMES sessions. Different EPCs subpopulations were quantified by cytometry markers CD34+/CD133+/CD45−, CD34+/CD133+/CD45−/VEGFR2 + and CD34+/CD45−/VEGFR2 +. Overall, CD34+/CD133+/CD45− EPCs increased from 13.5 ± 10.2 to 20.8 ± 16.9 and CD34+/CD133+/CD45−/VEGFR2 + EPCs from 3.8 ± 5.2 to 6.4 ± 8.5 cells/106 enucleated cells (mean ± SD, p < 0.05). CD34+/CD45−/VEGFR2 + EPCs also increased from 16.5 ± 14.5 to 23.8 ± 19.2 cells/106 enucleated cells (mean ± SD, p < 0.05). EPCs mobilization was not affected by NMES protocol and sepsis severity (p > 0.05), while it was related to corticosteroids administration (p < 0.05). NMES acutely mobilized endothelial progenitor cells, measures of the endothelial restoration potential, in septic ICU patients.

Alemtuzumab has been demonstrated to reduce the risks of relapse and accumulation of sustained disability in Multiple Sclerosis (MS) patients compared to β-interferon. It acts against CD52, leading primarily to lymphopenia. Recent data have shown that mild neutropenia is observed in 16% of treated MS-patients whereas severe neutropenia occurred in 0.6%. Herein, we present the case of a 34-year-old woman with relapsing-remitting MS, with a history of treatment with glatiramer acetate and natalizumab, who subsequently received Alemtuzumab (12 mg / 24 h × 5 days). 70-days after the last Alemtuzumab administration, the patient displayed neutropenia (500 neutrophils/μL) with virtual absence of B-cells (0.6% of total lymphocytes), low values of CD4-T-cells (6.6%) and predominance of CD8-T-cells (48%) and NK-cells (47%); while large granular lymphocytes (LGL) predominated in the blood-smear examination. Due to prolonged neutropenia (5-days) the patient was placed on low-dose corticosteroids leading to sustained remission. This is the first case of a patient with relapsing-remitting MS with neutropenia two months post-Alemtuzumab, with simultaneous presence of LGL cells in the blood and a robust therapeutic response to prednisolone. We recommend testing with a complete blood count every 15 days in the first 3 months after the 1st Alemtuzumab administration and searching for large granular lymphocytes cell expansion on microscopic examination of the peripheral blood if neutropenia develops.

Endothelial dysfunction and inflammation are common pathophysiological characteristics of chronic heart failure (CHF). Endothelial progenitor cells (EPCs) are recognized as useful markers of vascular damage and endothelial repair. The aim of this study was to investigate the effects of a cardiac rehabilitation program on EPCs and inflammatory profile in CHF patients of different severity. Forty-four patients with stable CHF underwent a 36-session cardiac rehabilitation program. They were separated into two different subgroups each time, according to the median peak VO₂, predicted peak VO₂, VE/VCO₂ slope, and ejection fraction. EPCs, C-reactive protein (CRP), interleukin 6 (IL-6), interleukin 10 (IL-10), and vascular endothelial growth factor (VEGF) were measured. Flow cytometry was used for the quantification of EPCs. Mobilization of EPCs increased and the inflammatory profile improved within each severity group (p < 0.05) after the cardiac rehabilitation program, but there were no statistically significant differences between groups (p > 0.05). A 36-session cardiac rehabilitation program has similar beneficial effects on the mobilization of EPCs and on the inflammatory profile in patients with CHF of different severity.

Rationale: Changes in anti-SARS-CoV-2 defense immune subsets in patients treated with dexamethasone (DXM) for severe COVID-19 and their relation to disease outcomes are poorly understood. Methods: Blood-lymphocyte subsets of 110 hospitalized COVID-19 patients were prospectively examined. A first sample was taken at enrollment and a second one 7–10 days later. Total B-, T-lymphocytes, CD4+, CD8+, T-regulatory (Treg), Natural-Killer (NK) and NK T-cells were counted using flow cytometry. Results: At enrollment, patients with respiratory failure, characterized by DXM failure (intubation/death) or DXM success (hospital discharge) exhibited significantly fewer CD3+, CD4+ and CD8+ cells and B-lymphocytes compared to the control group (no respiratory failure/no DXM). At the time of treatment completion, the DXM-failure group exhibited significantly fewer CD3+, CD4+ and CD8+ cells, memory CD4+ and CD8+ T-lymphocytes, compared to the control and the DXM-success groups and fewer activated CD4+ T-lymphocytes, Tregs and NK cells compared to the control group. At the time of treatment completion, the number of all investigated lymphocyte subsets increased in the DXM-success group and was similar to those of the control group. NK cells significantly decreased over time in the DXM-failure group. Conclusion: The lymphocyte kinetics differ between DXM-treated and control COVID-19 patients and are associated with clinical outcomes.

Endothelial progenitor cells (EPCs) constitute a cell population that enters the circulation during aerobic exercise and facilitates vascular function. In a similar action, hematopoietic progenitor cells (HPCs) are also released into circulation in response to exercise. Peripheral vascular dysfunction is frequently present in patients with heart failure. Whether acute interval exercise performed with high intensity induces EPC and HPC mobilization and affects microcirculation remains under investigation. The study population consisted of nineteen male patients with chronic heart failure (CHF) and eleven age-matched healthy individuals who underwent a high-intensity interval exercise session. Blood was drawn before, immediately after exercise, and 40 min after exercise to identify the numbers of circulating EPCs and HPCs by flow cytometry. Microcirculatory assessment was performed using near-infrared spectroscopy before and after exercise. Vascular endothelial growth factor (VEGF) change was also assessed before and after exercise in patients with CHF using flow cytometry. The interval exercise protocol revealed significant effects (p < 0.05) on EPC and HPC mobilization and systemic microcirculation (p < 0.05) in patients with CHF and healthy individuals. No significant differences were observed between patients with CHF and healthy individuals during interval exercise. VEGF did not reveal any changes immediately after interval exercise in CHF patients. Acute high-intensity interval training was associated with increased EPC and HPC mobilization and changes in microcirculation in patients with CHF and healthy individuals.