Lung microbiome and cytokine profiles in different disease states of COPD: a cohort study.

Increasing evidence indicates that respiratory tract microecological disorders may play a role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Understanding the composition of the respiratory microbiome in COPD and its relevance to respiratory immunity will help develop microbiome-based diagnostic and therapeutic approaches. One hundred longitudinal sputum samples from 35 subjects with acute exacerbation of COPD (AECOPD) were analysed for respiratory bacterial microbiome using 16S ribosomal RNA amplicon sequencing technology, and the sputum supernatant was analysed for 12 cytokines using a Luminex liquid suspension chip. Unsupervised hierarchical clustering was employed to evaluate the existence of distinct microbial clusters. In AECOPD, the respiratory microbial diversity decreased, and the community composition changed significantly. The abundances of Haemophilus, Moraxella, Klebsiella, and Pseudomonas increased significantly. Significant positive correlations between the abundance of Pseudomonas and TNF-α, abundance of Klebsiella and the percentage of eosinophils were observed. Furthermore, COPD can be divided into four clusters based on the respiratory microbiome. AECOPD-related cluster was characterized by the enrichment of Pseudomonas and Haemophilus and a high level of TNF-α. Lactobacillus and Veillonella are enriched in therapy-related phenotypes and may play potential probiotic roles. There are two inflammatory endotypes in the stable state: Gemella is associated with the Th2 inflammatory endotypes, whereas Prevotella is associated with the Th17 inflammatory endotypes. Nevertheless, no differences in clinical manifestations were found between these two endotypes. The sputum microbiome is associated with the disease status of COPD, allowing us to distinguish different inflammatory endotypes. Targeted anti-inflammatory and anti-infective therapies may improve the long-term prognosis of COPD.

MiR-144-3p inhibits the proliferation and metastasis of lung cancer A549 cells via targeting HGF.

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.

The value of apolipoprotein E in distinguishing benign and malignant unilateral pleural effusions.

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.