Purpose: Viral load of Torque Teno virus (TTV) is elevated in immunosuppressed patients. The weakened immune response is typical in chronic obstructive pulmonary disease (COPD) patients. However, the relationship between TTV and COPD is still unknown.Patients and Methods: We enrolled 91 patients admitted to hospitals with acute exacerbation of COPD (AECOPD) between January 2017 and August 2017 (ClinicalTrials.gov ID, NCT03236480). Sputum samples were gathered during hospitalization and the 120-day follow-up. TTV distribution and genogroups were assessed, and the associations between viral loads and clinical parameters were analyzed.Results: TTV DNA was detected in 95.6% of COPD patients, and the viral load was nearly invariable at the stable and exacerbation states. Most TTV DNA-positive patients carried four distinct genotypes. Sputum load of TTV was positively associated with RV/TLC (r = 0.378, p = 0.030), and negatively correlated with FEV1/pre and FEV1/FVC (r = −0.484, −0.432, p = 0.011, 0.024, respectively). Neutral correlation between the TTV DNA load and COPD assessment test (CAT) scores (r = 0.258, p = 0.018) was observed.Conclusion: Sputum loads of TTV DNA could be a novel indicator for lung function and disease severity assessment in COPD patients.
Background: T helper (Th) cell cytokine imbalances have been associated with the pathophysiology of chronic obstructive pulmonary disease (COPD), including the Th1/Th2 and Th17/T regulatory cells (Treg) paradigms. Clarifying cytokine profiles during COPD acute exacerbation (AE) and their relationships with clinical manifestations would help in understanding the pathogenesis of disease and improve clinical management. Materials and Methods: Eighty seven patients admitted to the hospital with AEs of COPD were included in this study, and follow-up was conducted after discharge (every 30 days, for a total of 120 days). Sputum samples of patients at different time points (including at admission, discharge, and follow-up) were collected, and sputum cytokine profiling (12 cytokines in total) was performed using a Luminex assay. Results: According to the cytokine profiles at admission, patients were divided into three clusters by a k-means clustering algorithm, namely, Th1 high Th17 high (n=26), Th1 low Th17 low (n=56), and Th1 high Th17 low (n=5), which revealed distinct clinical characteristics. Patients with Th1 high Th17 low profile had a significantly longer length of non-invasive ventilation time and length of hospital stay than patients with Th1 high Th17 high profile (7 vs 0 days, 22 vs 11 days, respectively, p < 0.05), and had the highest AE frequency. Sputum levels of Th17 cytokines (IL-17A, IL-22, and IL-23) during AE were negatively correlated with AE frequency in the last 12 months (r = −0.258, −0.289 and −0.216, respectively, p < 0.05). Moreover, decreased sputum IL-17A levels were independently associated with increased AE frequency, with an OR (95% CI) of 0.975 (0.958-0.993) and p = 0.006. Conclusion: Th1/Th17 imbalance during AE is associated with the severity of COPD. Decreased Th17 cytokine expression is correlated with increased AE frequency. The Th1/ Th17 balance may be a specific target for the therapeutic manipulation of COPD.
Background T helper (Th) cell cytokine imbalances have been associated with the pathophysiology of chronic obstructive pulmonary disease (COPD), including the Th1/Th2 and Th17/Treg paradigms. Clarifying cytokine profiles during COPD acute exacerbation (AE) and their relationships with clinical manifestations would help in understanding the pathogenesis of disease and improve clinical management.Methods Patients admitted to the hospital with AEs of COPD from January 2017 to August 2017 were included in this study, and follow-up was conducted after discharge (every 30 days, for a total of 120 days). Sputum samples of patients at different time points (including at admission, discharge, and follow-up) were collected, and sputum cytokine profiling (12 cytokines in total) was performed using a Luminex assay. Clinical data of patients were collected by a unified electronic medical record form.Results A total of 87 patients with COPD were enrolled, aged 72 ± 8.5 years, among whom 1, 12, 32, and 42 cases exhibited GOLD stage I, II, III, and IV, respectively. According to the cytokine profiles at admission, patients were divided into three clusters by a k -means clustering algorithm, namely, Th1 high Th17 high (n=26), Th1 low Th17 low (n=56), and Th1 high Th17 low (n=5), which revealed distinct clinical characteristics. Patients with Th1 high Th17 low profile had a significantly longer length of non-invasive ventilation time and length of hospital stay than patients with Th1 high Th17 high profile (7 vs. 0 days, 22 vs. 11 days, respectively, p < 0.05), and had the highest AE frequency. Sputum levels of Th17 cytokines (IL-17A, IL-22, and IL-23) during AE were negatively correlated with AE frequency in the last 12 months ( r = -0.258, -0.289 and -0.216, respectively, p < 0.05). Moreover, decreased sputum IL-17A levels were independently associated with increased AE frequency, whith an OR (95% CI) of 0.975 (0.958 - 0.993) and a p = 0.006.Conclusion Th1/Th17 imbalance during AE is associated with the severity of COPD. Decreased Th17 cytokine expression is correlated with increased AE frequency. The Th1/Th17 balance may be a specific target for the therapeutic manipulation of COPD.Trial registration: ClinicalTrials.gov ID: NCT03236480.
Aim MicroRNAs have been confirmed as vital regulators in gene expression, which could affect multiple cancer cell biological behaviors. This study aims to elucidate the molecular mechanism of miR-144-3p in lung cancer cellular proliferation and metastasis. Methods MiR-144-3p expression in lung cancer tissues and cell lines was detected by qRT-PCR. HGF was predicted as the target gene of miR-144-3p using TargetScan and dual luciferase reporter assay. Immunohistochemistry and qRT-PCR were used to explore the impacts of HCF on lung cancer tissues and cell lines. Impacts of miR-144-3p and HGF on cancer cellular proliferation, migration and invasion were elucidated by CCK-8, Flow cytometry, Transwell invasion and Wound-healing assay. Moreover, nude mouse xenograft model was established to evaluate the effects of miR-144-3p on lung cancer cells. Results MiR-144-3p exhibited a reduction in both lung cancer tissues and cell lines. HGF was a direct target of miR-144-3p. In contrast to the miR-144-3p expression level, HGF showed a higher level in lung cancer tissues and cell lines. Overexpression miR-144-3p suppressed A549 and NCI-H1299 cell proliferation and metastasis, whereas this was reversed by HGF. MiR-144-3p exhibited an inhibitory effect on A549 cell-induced tumor growth of nude mice. Conclusions This study reveals miR-144-3p/HGF axis may be involved in the suppression of lung cancer cellular proliferation and development, and miR-144-3p may function as a potential therapeutic target in lung cancer treatment in the future.
Pleural effusion (PE) remains insurmountable challenge and public health problem, requiring novel noninvasive biomarkers for accurate diagnosis. The aim of this study was to assess the clinical significance of apolipoprotein E (Apo-E) in PE, in order to determine its potential use as a diagnostic biomarker for malignant PE (MPE). PE samples were obtained from 127 patients and the etiology of PE was determined by multiple diagnostic techniques. Apo-E levels were then measured in the pleural fluid samples. 58 PE patients were diagnosed with tumors, while 69 were tumor-free. Apo-E levels in MPE patients were significantly higher than those with benign PE (BPE) (P < .05). An Apo-E cut-off of 69.96 ng/mL yielded sensitivity and specificity of 79.31% and 73.91% respectively for MPE detection. The area under the curve for Apo-E was 0.793 (95% confidence interval: 0.712 to 0.860), which was smaller than that of carcinoembryonic antigen (CEA) ( Z = 2.081, P< .05). In addition, the combination of Apo-E and CEA detection yielded a higher sensitivity of 87.90% and specificity of 95.65% in diagnosing MPE. In conclusion, Apo-E levels in PE may be a potential biomarker for the detection of MPE. The combined detection of Apo-E and CEA could improve the diagnostic sensitivity and specificity for MPE. These findings provide a simple and convenient method for clinical screening and detection of PE.
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