Oxidative stress caused by the production of reactive oxygen species (ROS) plays a major role in inflammatory processes. We hypothesized that modulation of ROS via quercetin may protect against oxidative stress and inflammation. Thus, this study aimed to investigate the effects of quercetin on oxidative stress and inflammation in lung epithelial A549 cells. The lipopolysaccharide (LPS)-induced elevation of intracellular ROS levels was reduced after quercetin treatment, which also almost completely abolished the mRNA and protein expression of nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2) induced by LPS stimulation. In addition, quercetin suppressed the nuclear translocation of nuclear factor kappa B (NF-κB) and reduced levels of inflammatory cytokine tumor necrosis factor (TNF)-α, interleukin (IL)-1, and IL-6, which had increased significantly after LPS exposure. Our data demonstrated that quercetin decreased ROS-induced oxidative stress and inflammation by suppressing NOX2 production.

Background: Pulmonary actinomycosis is a chronic pulmonary infection caused by Actinomyces. Both improving oral hygiene and early application of antibiotics to the case of suspicious pulmonary infections result in changes in incidences and presentations of pulmonary actinomycosis. However, there are little reports dealt with the recent clinical characteristics of pulmonary actinomycosis. This study aimed to review the characteristics of pulmonary actinomycosis occurred during the first decade of 21st century. Methods: This retrospective study was performed on 94 subjects with pulmonary actinomycosis diagnosed pathologically from January 2000 to December 2010 in 13 hospitals in Korea. Results: The data of the study showed that pulmonary actinomycosis occurs frequently in middle to old-aged males (mean age; 57.7 years old) and that the most common symptoms are cough, hemoptysis, and sputum production. Various radiologic features such as the consolidation with central low attenuation (74.5%) and no regional predominance were also observed. Most of patients recovered completely with medical and/or surgical treatment, reaching approximately 98% cure rate. Conclusions: The results demonstrate that pulmonary actinomycosis is one of the cautious pulmonary diseases. More importantly, in cases of persistent hemoptysis or for differential diagnosis from lung malignancy, our data have revealed that surgical resection appears to be a useful intervention and that radiologic diagnosis may not provide decisive information. These findings indicate that it is important for the clinicians to include pulmonary actinomycosis as one of differential diagnoses for refractory pulmonary abnormal lesions to the current usual management.

To assess the feasibility of xenon ventilation computed tomography (CT) for evaluating ventilation abnormality in asthmatics. Twenty-two, stable asthmatics (M:F = 10:12; mean age, 57.6) were included. Single-phase, whole-thorax, dual-energy CT was performed using dual-source CT (Somatom Definition, Siemens) after subjects had inhaled 30% xenon for 90 seconds. Parameters include 512 x 512 matrix; 14 x 1.2 mm collimation; 40/140 eff. mAs at 140/80 kV; 0.45 pitch; and 0.33 seconds rotation time. On the color-coded xenon map, the extent of the ventilation defect was visually assessed using a 5-point scale in each lobe (0, absent defect; 1, 0%-25%; 2, 25%-50%; 3, 50%-75%; and 4, 75%-100%), which was defined as defect score. On the weighted average image, airway wall dimensions were measured at 4 segmental bronchi in both upper and lower lobes. Patients were classified into a defect group and a defect-free group based on the presence of defects shown on the xenon map. Pulmonary function test parameters and airway wall dimensions were compared in those 2 groups. Correlation analyses between the defect score, pulmonary function test, and airway wall dimensions were performed. Sixteen asthmatics showed peripheral ventilation defects on the xenon map (defect score, 6.6 +/- 4.2). The defect group had a significantly lower forced expiratory volume in 1 second (FEV1) and thicker airway wall than that of the defect-free group (P = 0.04 and 0.02, respectively). The defect score correlated negatively with a ratio of FEV1 and forced vital capacity (FEV1/FVC) (r = -0.44, P = 0.04) and corrected diffusing capacity (r = -0.76, P = 0.04) and correlated positively with total lung capacity, functional residual volume, and residual volume (r = 0.90, P = 0.005; r= 0.99, P < 0.001; r = 0.88, P = 0.008, respectively). The ventilation defects appeared on xenon ventilation CT in asthmatics with more severe airflow limitation and airway wall thickening. The extent of the ventilation defects showed correlations with parameters of pulmonary function test.

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive interstitial lung disease of unknown cause which leads to alveolar epithelial cell apoptosis followed by basement membrane disruption and accumulation of extracellular matrix, destroying the lung architecture. Oxidative stress is involved in the development of alveolar injury, inflammation, and fibrosis. Oxidative stress‐mediated alveolar epithelial cell (AEC) apoptosis is suggested to be a key process in the pathogenesis of IPF. Therefore, the present study investigated whether grape seed proanthocyanidin extract (GSPE) could inhibit the development of pulmonary fibrosis via ameliorating epithelial apoptosis through the inhibition of oxidative stress. We found that GSPE significantly ameliorated the histological changes and the level of collagen deposition in bleomycin (BLM)‐induced lungs. Moreover, GSPE attenuated lung inflammation by reducing the total number of cells in bronchoalveolar lavage (BAL) fluid and decreasing the expression of IL‐6. We observed that the levels of H₂O₂ leading to oxidative stress were increased following BLM instillation, which significantly decreased with GSPE treatment both in vivo and in vitro. These findings showed that GSPE attenuated BLM‐induced epithelial apoptosis in the mouse lung and A549 alveolar epithelial cell through the inhibition of oxidative stress. Furthermore, GSPE could attenuate mitochondrial‐associated cell apoptosis via decreasing the Bax/Bcl‐2 ratio. The present study demonstrates that GSPE could ameliorate bleomycin‐induced pulmonary fibrosis in mice via inhibition of epithelial apoptosis through the inhibition of oxidative stress.

Lee YS, et al. J Korean Med Sci. 2013 Jul;28(7):1048-1054. https://doi.org/10.3346/jkms.2013.28.7.1048

Background: To date, no clinical parameter has been associated with the decline in lung function other than emphysema severity in COPD. Objectives: The main purpose of this study was to explore whether the rate of lung function decline differs between COPD patients with and without exertional desaturation. Methods: A total of 224 subjects were selected from the Korean Obstructive Lung Disease cohort. Exertional desaturation was assessed using the 6-min walk test (6MWT), and defined as a post-exercise oxygen saturation (SpO₂) of <90% or a ≥4% decrease. The cohort was divided into desaturator (n = 47) and non-desaturator (n = 177) groups. Results: There was a significant difference between the desaturator and non-desaturator groups in terms of the change in pre-bronchodilator forced expiratory volume in 1 s (FEV₁) over a 3-year period of follow-up (p = 0.006). The mean rate of decline in FEV₁ was greater in the desaturator group (33.8 ml/year) than in the non-desaturator group (11.6 ml/year). A statistically significant difference was also observed between the two groups in terms of the change in the St. George's Respiratory Questionnaire (SGRQ) total score over 3 years (p = 0.001). Conclusions: This study suggests, for the first time, that exertional desaturation may be a predictor of rapid decline in lung function in patients with COPD. The 6MWT may be a useful test to predict a rapid lung function decline in COPD.