Immunophenotyping of Monocyte Migration Markers and Therapeutic Effects of Selenium on IL-6 and IL-1ß Cytokine Axes of Blood Mononuclear Cells in Preoperative and Postoperative Coronary Artery Disease Patients.

Multivessel coronary artery disease (CAD) is characterized by underlying chronic vascular inflammation and occlusion in the coronary arteries, where these patients undergo coronary artery bypass grafting (CABG). Since post-cardiotomy inflammation is a well known phenomenon after CABG, attenuation of this inflammation is required to reduce perioperative morbidity and mortality. In this study, we aimed to phenotype circulating frequencies and intensities of monocyte subsets and monocyte migration markers, respectively, and to investigate the plasma level of inflammatory cytokines and chemokines between preoperative and postoperative CAD patients and later, to intervene the inflammation with sodium selenite. We found a higher amplitude of inflammation, postoperatively, in terms of CCR1high monocytes and significantly increased pro-inflammatory cytokines, IL-6, IL-8, and IL-1RA. Further, in vitro intervention with selenium displayed mitigating effects on the IL-6/STAT-3 axis of mononuclear cells derived from postoperative CAD patients. In addition, in vitro selenium intervention significantly reduced IL-1ß production as well as decreased cleaved caspase-1 (p20) activity by preoperative (when stimulated) as well as postoperative CAD mononuclear cells. Though TNF-α exhibited a positive correlation with blood troponin levels in postoperative CAD patients, there was no obvious effect of selenium on the TNF-α/NF-κB axis. In conclusion, anti-inflammatory selenium might be utilized to impede systemic inflammatory cytokine axes to circumvent aggravating atherosclerosis and further damage to the autologous bypass grafts during the post-surgical period.

Outcomes of patients with coronavirus disease versus other lung infections requiring venovenous extracorporeal membrane oxygenation.

Background: Patients with Coronavirus Disease (COVID-19) often develop severe acute respiratory distress syndrome (ARDS) requiring prolonged mechanical ventilation (MV), and venovenous extracorporeal membrane oxygenation (V-V ECMO).Mortality in COVID-19 patients on V-V ECMO was exceptionally high; therefore, whether survival can be ameliorated should be investigated. Methods: We collected data from 85 patients with severe ARDS who required ECMO support at the University Hospital Magdeburg from 2014 to 2021. The patients were divided into the COVID-19 group (52 patients) and the non-COVID-19 group (33 patients). Demographic and pre-, intra-, and post-ECMO data were retrospectively recorded. The parameters of mechanical ventilation, laboratory data before using ECMO, and during ECMO were compared. Results: There was a significant difference between the two groups regarding survival: 38.5% of COVID-19 patients and 63.6% of non-COVID-19 patients survived 60 days (p = 0.024). COVID-19 patients required V-V ECMO after 6.5 days of MV, while non-COVID-19 patients required V-V ECMO after 2.0 days of MV (p = 0.048). The COVID-19 group had a greater proportion of patients with ischemic heart disease (21.2% vs 3%, p = 0.019). The rates of most complications were comparable in both groups, whereas the COVID-19 group showed a significantly higher rate of cerebral bleeding (23.1 vs 6.1%, p = 0.039) and lung bacterial superinfection (53.8% vs 9.1%, p = <0.001). Conclusion: The higher 60-days mortality among patients with COVID-19 with severe ARDS was attributable to superinfection, a higher risk of intracerebral bleeding, and the pre-existing ischemic heart disease.

Ghrelin Exerts Analgesic Effects through Modulation of IL-10 and TGF-ß Levels in a Rat Model of Inflammatory Pain.

BACKGROUND: Ghrelin is a peptide with attenuating effect on inflammatory pain. Both anti- and pro-inflammatory mediators have a role in the nociception and development of pain and hyperalgesia. IL-10 and TGF-ß are anti-inflammatory cytokines and inhibit the expression of pro-inflammatory cytokines related to peripheral and central inflammatory pain. In this study, the effects of i.p. injection of ghrelin on the early and the late phases of pain, as well as serum levels of IL-10 and TGF-ß, as anti-inflammatory cytokines, were investigated in formalin-induced pain in male rats. METHODS: Adult male Wistar rats (n=48) were randomly divided into six groups: control, formalin+saline, ghrelin (40, 80, and 160 µg/kg), and morphine. Ghrelin was administered i.p. 30 min before inducing pain by formalin. Pain induced by intraplantar (i.pl.) injection of 50 µl formalin 5%, and pain behavior was studied for 60 min. Serum IL-10 and TGF-ß levels were assessed by ELISA method. RESULTS: The findings of the present study showed that ghrelin with high doses (80 and 160 µg/kg) significantly reduced pain intensity in both the early and the late phases of pain. The serum levels of cytokines, IL-10, and TGF-ß1 showed a significant elevation with ghrelin at the dose of 160 µg/kg. CONCLUSION: Ghrelin is effective in reducing the intensity of both the early and the late phases of inflammatory pain. It seems that ghrelin exerts its analgesic effects in part by increasing the serum levels of anti-inflammatory cytokines.