Chronic Obstructive Pulmonary Disease Patients With High Peripheral Blood Eosinophil Counts Have Better Predicted Improvement in 6MWD After Rehabilitation: A PRELIMINARY STUDY.

PURPOSE: The objective of this investigation was to determine whether chronic obstructive pulmonary disease (COPD) patients with high blood eosinophil (EOS) counts had better improvement in 6-min walk test (6MWT) after pulmonary rehabilitation (PR). METHODS: Fifty COPD patients were randomly assigned to either the rehabilitation group (RG) or the control group (CG). Patients in the RG (8 wk PR + routine medication) and the CG (routine medication) were followed for 32 wk. According to the blood EOS level, the RG was divided into an EOS ≥ 200 cells/µL group and EOS < 200 cells/µL group. The 6MWT distance, Borg Scale, and COPD Assessment Test (CAT) were evaluated before intervention and 8 wk and 32 wk later. RESULTS: After the 8-wk intervention, 37 patients (19 RG/18 CG) completed the study. At 8-wk and 32-wk follow-up from baseline, a statistically significant difference was found between these two groups in the 6MWT, Borg Scale, and CAT. Compared with baseline, the 6MWT in the RG increased 49.1 ± 40.2 m (95% CI, 29.7-68.5, P < .001) at 8 wk and 60.8 ± 42.1 m (95% CI, 40.5-81.6, P < .001) at 32 wk. In addition, the improvement of 6MWT in the EOS ≥ 200 cells/µL RG group was higher than that in the EOS < 200 cells/µL group (40.1 ± 17.6 m, 95% CI, 36.8-43.4; P = .036) at 32-wk follow-up from baseline. CONCLUSION: An 8-wk PR can improve the exercise capacity of COPD patients, and the benefits persistent for 24 wk. The improvement in the 6MWT was more significant in COPD patients with a high blood EOS count.

Cigarette smoke extract alters the cell cycle via the phospholipid transfer protein/transforming growth factor-ß1/CyclinD1/CDK4 pathway.

This study was aimed to investigate the effect of phospholipid transfer protein (PLTP) on cigarette smoke extract (CSE)-induced alteration of the cell cycle and the possible mechanism. Male Wistar rats and the rat alveolar epithelial cell line (RLE-6TN) were exposed to normal air or different concentrations of CSE. Then PLTP siRNA was transfected into cells and an inhibitor of transforming growth factor-ß1 (TGF-ß1) was administered prior to CSE exposure. Histological changes and cell cycle stage were recorded, as were the expression levels of PLTP, TGF-ß1, CyclinD1 and CDK4. Resulting morphological changes included diffuse interstitial substance incrassation and elevated alveolar rupturing. Flow cytometry analysis revealed an increase in the number of cells in the G1 phase in a time- and dose-related manner. Both PLTP and TGF-ß1 were up-regulated at protein and mRNA levels, whereas CyclinD1 and CDK4 expression was down-regulated after CSE exposure. Furthermore, PLTP siRNA significantly suppressed CSE-induced TGF-ß1 expression, resulting in up-regulation of CyclinD1 and CDK4, but the TGF-ß1 inhibitor was not able to abrogate CSE-induced PLTP over-expression. In conclusion, PLTP may operate upstream of the TGF-ß1/CyclinD1/CDK4 pathway and may mediate the CSE-induced G1 arrest in RLE-6TN cells. Our work provides some new insight into the relation between PLTP and cell cycle progression.