[Correlation between systemic inflammation level and emphysema degree and bone mineral density in chronic obstructive pulmonary disease patients and its mechanism].

Objective: To study the correlation between systemic inflammation level and emphysema degree and bone mineral density in chronic obstructive pulmonary disease (COPD) patients and its possible mechanism. Methods: 90 patients with stable COPD who met the inclusion criteria and 50 controls in the physical examination center during the same period were recruited. All the enrolled objects have collected general clinical data, analyzed peripheral blood samples, measuring the Low-attenuation area of lung and CT value of lumbar 1 vertebra (L1-CT) by chest spiral CT. According to LAA%, COPD patients were divided into 36 cases of the non-emphysema group, 32cases of mild to moderate emphysema group, and 22 cases of severe emphysema group. The correlation between L1-CT value, LAA%, peripheral blood inflammatory factors, and pulmonary function indices in each group was analyzed and compared. Results: The HU value of L1-CT (107±32) in the COPD group was significantly lower than that in the control group (153±30), and the difference was statistically significant (P<0.05). The higher the LAA% in COPD patients was, the lower the value of L1-CT was, and the difference between groups was statistically significant. Compared with COPD patients in the non-emphysema group, peripheral blood neutrophil/lymphocyte ratio (NLR), platelet/lymphocyte ratio (PLR), and C-reactive protein (CRP) were all increased in the emphysema group, and the differences were statistically significant (P<0.05). L1-CT was negatively correlated with LAA, PLR, NLR, and CRP while uncorrelated with serum concentration of calcium and phosphorus. Conclusion: The decrease in bone density in COPD patients is closely related to the degree of emphysema. It is associated with increased levels of systemic inflammation caused by COPD itself. Early and timely broad-spectrum anti-inflammatory treatment may have certain clinical significance for the prevention and treatment of comorbidity with osteoporosis.

[Influenza virus activates toll-like receptor 7/nuclear factor-κB signaling pathway to regulate airway inflammatory response in patients with acute exacerbation of chronic obstructive pulmonary diseases].

Objective: To explore how influenza A virus (IAV) regulates airway inflammation via activating Toll-like receptor 7(TLR7)/nuclear factor of κB (NF-κB) signaling pathway in patients with acute exacerbation of chronic obstructive pulmonary disease (COPD). Methods: Primary bronchial epithelial cells were isolated and cultured from normal controls and COPD patients. Samples were divided into 6 groups according to different in vitro treatment, including normal epithelial cell group (A), normal cells+IAV group (B), COPD epithelial cell group (C), COPD cells+IAV group (D), normal cells+TLR7 small interference RNA (si-RNA) group (E), COPD cells+TLR7 siRNA group (F). Protein expressions of TLR7 and NF-κB were detected by Western blot after 24h co-culture with IAV and TLR7 siRNA. Interleukin-6 (IL-6) and tumor necrosis factor α (TNF α) were detected by enzyme-linked immunosorbent assay (ELISA). Results: (1) Compared with group A [0.350±0.075 and 0.470±0.034, (53.000±6.532)pg/ml and (17.000±1.625)pg/ml],TLR7, NF-κB protein expression and IL-6, TNF α levels were significantly increased in group B[0.950±0.075 and 1.090±0.078,(185.000±7.874)pg/ml and (32.000±0.838)pg/ml], group C[0.780±0.056 and 0.910±0.045,(138.000±5.100)pg/ml and 29.000±1.323)pg/ml) and group D[1.280±0.031 and 1.540±0.051,(432.000±5.734)pg/ml and (52.000±3.453)pg/ml] (all P<0.01). Compared with group C TLR7, NF-κB protein expression and IL-6, TNF α levels were significantly increased in group D (P<0.01). (2) Compared with the group A[0.530±0.023 and 0.800±0.046,(51.000±0.327)pg/ml and (14.000±0.314)pg/ml], TLR7, NF-κB protein expression and IL-6, TNF α levels were significantly decreased in the group E[0.350±0.047 and 0.510±0.067,(26.000±1.081)pg/ml and(8.000±0.526)pg/ml] (P<0.05). Compared with group C[1.080±0.078 and 1.280±0.034,(125.000±2.249)pg/ml and (28.000±1.010)pg/ml], TLR7, NF-κB protein expression and IL-6, TNF α levels decreased in the group F[0.880±0.056 and 1.040±0.029,(83.000±1.125)pg/ml and (21.000±0.429)pg/ml] (P<0.05). Conclusion: Influenza viruses activate TLR7/NF-κB signaling pathway to regulate airway inflammation storms in patients with acute exacerbation of COPD. New therapeutic targets of acute exacerbation COPD may be studied based on these inflammation responses to influenza viruses.

[Association of sleep-disorders with systemic inflammatory markers and acute exacerbation in chronic obstructive pulmonary disease patients].

Objective: To investigate the association of sleep quality with the levels of systemic inflammatory markers in patients with chronic obstructive pulmonary disease(COPD) and the correlations between the frequency of acute exacerbation of COPD (AECOPD) and Pittsburgh sleep quality index (PSQI). Methods: A total of 198 COPD patients admitted in our hospital from October, 2016 to June, 2017 were screened, and 124 patients were eligible for the study. On the first day of hospitalization, the serum samples and clinical data were collected, including white blood cells, lymphocytes, platelet count, CRP and PSQI. Poor sleep quality was defined as PSQI score >5. Results: The percentage of COPD patients with poor sleep quality was about 68%. Poor sleep quality was positively correlated with the frequency of acute exacerbation in COPD patients. The ratio of neutrophil to lymphocyte (NLR), ratio of platelet to lymphocyte (PLR) and levels of CRP were higher in patients with poor sleep quality than those in the control group. NLR, PLR and CRP in peripheral blood of the patients with poor sleep quality were positively correlated with PSQI score. The CRP levels and PSQI score in COPD patients with poor sleep quality group were positively correlated with the frequency of exacerbations in the past year (r=0.437, r=0.430). Conclusion: A high percentage of COPD patients had poor sleep quality, which was positively correlated with the levels of systemic inflammation as well as the frequency of AECOPD.

Chronic hypoxia-induced alteration of presynaptic protein profiles and neurobehavioral dysfunction are averted by supplemental oxygen in Lymnaea stagnalis.

Chronic hypoxia causes neural dysfunction. Oxygen (O(2)) supplements have been commonly used to increase the O(2) supply, yet the therapeutic benefit of this treatment remains controversial due to a lack of cellular and molecular evidence. In this study, we examined the effects of short-burst O(2) supplementation on neural behavior and presynaptic protein expression profiles in a simple chronic hypoxia model of snail Lymnaea stagnalis. We reported that hypoxia delayed the animal response to light stimuli, suppressed locomotory activity, induced expression of stress-response proteins, hypoxia inducible factor-1alpha (HIF-1alpha) and heat shock protein 70 (HSP70), repressed syntaxin-1 (a membrane-bound presynaptic protein) and elevated vesicle-associated membrane protein-1 (VAMP-1) (a vesicle-bound presynaptic protein) level. O(2) supplements relieved suppression of neural behaviors, and corrected hypoxia-induced protein alterations in a dose-dependent manner. The effectiveness of supplemental O(2) was further evaluated by determining time courses for recovery of neural behaviors and expression of stress response proteins and presynaptic proteins after relief from hypoxia conditions. Our findings suggest that O(2) supplement improves hypoxia-induced adverse alterations of presynaptic protein expression and neurobehaviors, however, the optimal level of O(2) required for improvement is protein specific and system specific.