Correlation Analysis of Blood Glucose Level with Inflammatory Response and Immune Indicators in Patients with Sepsis.

Objective: To analyze the correlation of blood glucose level with inflammatory response and immune indicators in patients with sepsis. Methods: Between February 2019 and February 2021, 30 sepsis patients and 30 sepsis patients complicated with diabetes mellitus admitted to our hospital were recruited and assigned to either the experimental group (sepsis patients) or the observation group (sepsis patients with diabetes mellitus). Another 30 healthy subjects in the same period were included as the control group. The levels of IL-6, TNF-α, IL-1ß, CD4+, and CD8+ in the three groups of patients were compared to analyze the correlation of blood glucose levels with inflammatory response and immune indicators in patients with sepsis. The difference of counting data was analyzed using the chi-square test, and the difference of measurement data was analyzed using the t-test. Results: The control group showed the lowest levels of IL-6 at 14.32 ± 4.98 pg/ml, followed by 18.33 ± 3.27 pg/ml in the experimental group and then 22.64 ± 5.16 pg/ml in the observation group (P < 0.05). The levels of other inflammatory factors including TNF-α and IL-1ß were the lowest in the control group, followed by the experimental group, and then the observation group (P < 0.05). The lowest immune function indicator CD4+ and CD8+ levels were found in the observation group, followed by the experimental group, and then the control group (P < 0.05). The blood glucose level of patients with sepsis was positively correlated with the levels of IL-6, TNF-α, and IL-1ß and was negatively correlated with the levels of CD4+/CD8+. The higher the blood glucose, the lower the number of immune cells. Conclusion: The blood glucose level of patients with sepsis is positively correlated with inflammatory response and negatively with immune indicators. An increased blood sugar level is associated with aggravated inflammatory responses and a decreased number of immune cells, which provides a reference for the disease severity assessment and treatment of patients with sepsis.

Efficacy of Oxymatrine Plus Antiviral in the Treatment of Sepsis and Its Effect on the Levels of Endotoxin and Inflammatory Factors.

Objective: To assess the clinical efficacy of oxymatrine plus antiviral therapy in the treatment of sepsis and its effects on the levels of endotoxin and inflammatory factors. Methodology. 90 patients with sepsis were selected for retrospective analysis and were assigned to receive either conventional treatment (control group) or oxymatrine plus antiviral treatment (study group). The clinical endpoint was treatment efficacy. Results: There were no significant differences in baseline patient profile between the two groups (P > 0.05). The study group showed a higher efficiency versus the control group (P < 0.05). Patients in the study group had a significantly shorter mechanical ventilation duration and ICU stay versus those in the control group (P < 0.05). Both groups had reduced Acute Physiology and Chronic Health Evaluation II (APACHE II) score, Marshall score, levels of endotoxin, tumor necrosis factor-α (TNF-α), interleukin (IL)-6, IL-8, C-reactive protein (CRP), and procalcitonin (PCT) after treatment, with lower results in the study group versus the control group (P < 0.05). Conclusion: Oxymatrine plus antiviral therapy effectively improves clinical efficacy, reduces the levels of endotoxin and inflammatory factors, protects organ function, and boosts recovery. Further clinical trials are, however, required prior to general application in clinical practice.

Potential of circulating lncRNA CASC2 as a biomarker in reflecting the inflammatory cytokines, multi-organ dysfunction, disease severity, and mortality in sepsis patients.

BACKGROUND: Long noncoding RNA (lncRNA) cancer susceptibility candidate gene 2 (CASC2) inhibits inflammation and multi-organ dysfunction in various ways. The present study was intended to explore the potency of blood lncRNA CASC2 as a biomarker for sepsis management. METHODS: Totally, 184 sepsis patients and 30 healthy controls were enrolled. The reverse transcription-quantitative polymerase chain reaction was used to detect lncRNA CASC2 expression in peripheral blood mononuclear cell samples from the subjects. Mortality during 28 days was recorded in sepsis patients. RESULTS: LncRNA CASC2 was decreased in sepsis patients [median (interquartile range [IQR]): 0.473 (0.241-0.773)] by comparison to healthy controls [median (IQR): 1.019 (0.676-1.685)] (p < 0.001). In sepsis patients, lncRNA CASC2 was negatively correlated with Acute Physiology and Chronic Health Evaluation II (APACHE II) (p = 0.001), Sequential Organ Failure Assessment (SOFA) (p < 0.001), SOFA-respiratory system (p = 0.010), SOFA-coagulation (p = 0.020), SOFA-liver (p = 0.019), and SOFA-renal (p = 0.010) scores, but was not related to SOFA-nervous (p = 0.466) and SOFA-cardio vascular system (p = 0.059) scores. Additionally, lncRNA CASC2 was negatively related to tumor necrosis factor-α (p = 0.024), interleukin (IL)-1ß (p = 0.013), and IL-17A (p = 0.002), but was not linked to IL-6 (p = 0.112) or IL-10 (p = 0.074). Furthermore, lncRNA CASC2 was lower in sepsis deaths [median (IQR): 0.286 (0.166-0.475)] than in survivors [median (IQR): 0.534 (0.296-0.811)] (p < 0.001). Simultaneously, Kaplan-Meier (KM) curve analysis also observed that lncRNA CASC2 was inversely related to accumulating mortality in sepsis patients (p = 0.003). While lncRNA CASC2 could independently predict lower mortality risk. CONCLUSION: Circulating lncRNA CASC2 inadequacy indicates the release of inflammatory cytokines, severe multi-organ injuries, and increased mortality in sepsis patients.

Increased miR-21a provides metabolic advantages through suppression of FBP1 expression in non-small cell lung cancer cells.

Lung cancer is the most common solid tumor and the leading cause of cancer-related mortality worldwide. miR-21 is one of the most commonly observed aberrant miRNAs in human cancers. However, the biological roles of miR-21 in glucose metabolism of non-small cell lung cancer (NSCLC) cells remain unknown. In the present study, our findings demonstrated that miR-21 promoted glucose uptake and increased TXNIP expression. miR-21 increased lactate generation and decreased oxygen consumption in NSCLC cells. Moreover, we found that miR-21 promoted glycolysis and decreased OXPHOS. Mechanistically, fructose-1,6-biphosphatase (FBP1) was a direct target of miR-21 and observed a negative correlation between miR-21 and FBP1 in NSCLC samples. Restoring FBP1 expression reversed the effects induced by miR-21 overexpression in NSCLC cells. Together, our findings suggest the critical role of miR-21 in glucose metabolism through suppression of FBP1 in NSCLC cells. miR-21 may be a potential target of NSCLC treatment.

Diagnostic value of elevated serum miRNA-143 levels in sepsis.

OBJECTIVE: To evaluate serum micro RNA-143 (miR-143) levels in patients with sepsis or non-infectious systemic inflammatory response syndrome (SIRS), and investigate its possible diagnostic or prognostic value. METHODS: Serum was obtained from patients with sepsis or SIRS and healthy control subjects. Relative miR-143 expression was determined using quantitative real time polymerase chain reaction. The diagnostic and prognostic value of serum miR-143 was evaluated. RESULTS: Serum miR-143 levels were significantly higher in patients with sepsis (n = 103) than patients with SIRS (n = 95) and healthy controls (n = 40). There were significant positive correlations between serum miR-143 level and SOFA and APACHE II scores in patients with sepsis (r = 0.794 and r = 0.825, respectively). Serum miR-143 had a sensitivity of 78.6% and specificity of 91.6% for distinguishing between sepsis and SIRS. There was no association between serum miR-143 and 28-day survival in patients with sepsis. CONCLUSION: Serum miR-143 is elevated in patients with sepsis, and may be a useful biomarker for distinguishing between sepsis and SIRS.

Hydrogen-rich saline ameliorates lung injury associated with cecal ligation and puncture-induced sepsis in rats.

AIMS: Although hydrogen has been proved to be a novel therapeutic medical gas in several lung injury animal models, to our knowledge, it has not been tested yet in acute lung injury (ALI) induced by cecal ligation and puncture (CLP). This study was to investigate the hypothesis that hydrogen could ameliorate CLP-induced lung injury in rats. METHODS AND RESULTS: Our experiments exhibited that gas exchange dysfunction and lung tissue inflammation were observed in animals exposed to CLP. Hydrogen-rich saline treatment significantly attenuated lung injury as indicated by significantly improved gas exchange and histological changes in the lung and significantly reduced lung water content (LWC) and neutrophil infiltration 8h after CLP. Lipid peroxidation and DNA oxidation in the lung tissue were significantly reduced along with a decreased nitrotyrosine content and maintained superoxide dismutase activity in the presence of hydrogen, demonstrating antioxidant role of hydrogen in CLP-induced ALI. Importantly, hydrogen-rich saline treatment significantly inhibited the activation of p-p38 and NF-κB while suppressing the production of several proinflammatory mediators. CONCLUSIONS: This observation indicated that hydrogen-rich saline peritoneal injection improves histological and functional assessment in rat model of CLP-induced ALI. The therapeutic effects of hydrogen-rich saline may be related to antioxidant and anti-inflammatory actions.

Neutrophils in acute lung injury.

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is characterised by lung oedema due to increased permeability of the alveolar-capillary barrier and subsequent impairment of arterial oxygenation. Lung oedema and endothelial and epithelial injury are accompanied by an influx of neutrophils into the interstitium and alveolar space. Hence, the activation and recruitment of polymorphonuclear neutrophils (PMNs) are thought to play key roles in the progression of ALI/ARDS. Neutrophils, which have anti-microbial activity, are the first cells to be recruited to the site of inflammation. This review focuses on the mechanisms of neutrophil activity in patients with ALIs with respect to attachment, recruitment, adhesion, migration, activation, release of damage mediators, and apoptosis via PMNs.