Background Chronic obstructive pulmonary disease (COPD) is a prevalent, progressive respiratory disease, and acute exacerbations of COPD (AECOPD) can accelerate the deterioration of the disease. Increasing evidence suggests that airway bacterial dysbiosis is associated with AECOPD. However, the exact relationship between changes in the sputum microbiome during AECOPD and clinical indices remains unclear. Methods In this study, a total of 76 sputum samples were collected from patients with AECOPD (n = 28), stable COPD (n = 23), recovery (n = 15) and healthy controls (HCs; n = 10). The sputum microbiome profile was analysed by sequencing the V3‑V4 amplicon of the 16S rRNA (ribosomal RNA) gene. Results The bacterial diversity (Shannon and Simpson’s index) was found to be significantly decreased in the AECOPD and recovery groups when compared to that in the stable COPD and HC groups. The most dominant phylum identified in the sputum samples of AECOPD patients was Proteobacteria, accounting for 30% of the microbiome. Compared to the stable COPD groups, the relative abundances of Firmicutes and Bacteroidetes were decreased, whereas those of Proteobacteria and Actinobacteria were increased in AECOPD patients. Furthermore, discriminative bacteria, such as Haemophilus, were identified as being specific taxa in AECOPD patients. Functional analysis showed that genes involved in membrane transport and signal transduction metabolism were enriched in the AECOPD group. Importantly, the proportions of Veillonella were positively correlated with lung function, and Staphylococcus was positively correlated with inflammatory indices. Conclusion Our study revealed variations in the sputum microbiome of AECOPD (based on composition and function) in a Chinese cohort and highlighted its correlation to clinical indices. These results indicated that microbial dysbiosis may contribute to disease progression and provide microbial biomarkers for the diagnosis of AECOPD.
Purpose In this study, we aimed to investigate the precise relationship between hypoxia-inducible factor 1α (HIF1α), circadian clock genes, and OSA. Methods We recruited 21 patients with OSA and 22 age-matched controls who underwent polysomnography and had their peripheral blood collected on the evening before and the morning after sleep. OSA was defined as an apnea hypopnea index (AHI) ≥15 events/h. Patients in which T90 > 0 were defined as having nocturnal hypoxemia (NH) and were referred to as the NH group. The mRNA levels of HIF1α, HIF1β and several clock genes ( Timeles s, Clock, Bmal1, Per1, Per2, Per3, Cry1, Cry2, Ck1δ, Rorα, NR1D1 , and NPAS2) were determined by RT-qPCR. The percentage difference in gene expression levels when compared between the morning and evening was then determined as referred to as morning-evening variation (MEV). Results The MEV for HIF1α mRNA expression in OSA patients increased significantly by 23% ( P = 0.008) when compared to patients without OSA. The gene expression levels of Timeless ( P = 0.038) and Cry2 ( P = 0.012) decreased with AHI. The MEV of Bmal1, Rorα , and HIF1α mRNA levels were upregulated by 16% ( P = 0.006), 14% ( P = 0.027), and 25% ( P = 0.005), respectively, in participants with NH when compared to those without NH. Furthermore, the MEV for HIF1α mRNA levels was positively correlated with the MEV of Bmal1, Cry1 , and CK1δ mRNA levels ( R = 0.638, P < 0.001; R = 0.327, P = 0.002; R = 0.332, P = 0.001, respectively) and negatively correlated with LSpO 2 ( R = −0.464, P =0.009) and Mean SpO 2 ( R = −0.500, P = 0.003). Conclusion Our data suggest that patients with OSA or NH tend to develop circadian rhythm disorders that may be induced by the hypoxia-mediated augmentation of HIF1α gene expression in OSA.
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