Indeed, decreased α1-antitrypsin levels in BEAS-2B cells suggest that exposure to PS-MPs increases the risk for chronic obstructive pulmonary disease, and high concentrations of PS-MPs can induce these adverse responses.
Both miR-34c-5p agomir and CCL22 shRNA could reduce breathing frequency (f), airway resistance (RI), and the levels of IL-8 and TNF-α in BALF of COPD rats with increased Cydn (dynamic lung compliance) and PIF (peak inspiratory flow).
Both miR-34c-5p agomir and CCL22 shRNA could reduce breathing frequency (f), airway resistance (RI), and the levels of IL-8 and TNF-α in BALF of COPD rats with increased Cydn (dynamic lung compliance) and PIF (peak inspiratory flow).
Other inflammatory pathways are also emerging as implicated in asthma and COPD molecular phenotypes, including Type one and Type 17 adaptive immune responses and proinflammatory cytokines, such as interleukin-6.
Our results suggest that cigarette smoke-induced airway inflammation and small airway remodeling are partially mediated by 5-HTR2A and 5-HTR2B, which could be a new therapeutic target for airway remodeling in COPD.
TGF-β1 is increased in chronic obstructive pulmonary disease (COPD), and known to decrease the expression of constitutive host defense mediators such as secretory leukocyte protease inhibitor (SLPI) and polymeric immunoglobulin receptor (pIgR).
Meta-analysis results indicated that age (OR = 1.29, 95% CI 1.06-1.58, P = 0.01), smoking (OR = 1.62, 95% CI 1.27-2.07, P < 0.01), COPD (chronic obstructive pulmonary disease) (OR = 1.62, 95% CI 1.19-2.22, P < 0.01), CAD (coronary atherosclerotic heart disease) (OR = 1.82, 95% CI 1.36-2.45, P < 0.01), T-stage (OR = 0.81, 95% CI 0.67-0.98, P = 0.03), previous radiotherapy (OR = 2.41, 95% CI 2.00-2.90, P < 0.01), preoperative albumin (OR = 2.95, 95% CI 1.47-5.91, P < 0.01), preoperative hemoglobin (OR = 1.97, 95% CI 1.28-3.03, P < 0.01), tumor site (OR = 0.28, 95% CI 0.22-0.36, P < 0.01), and treatment method (OR = 1.85, 95% CI 1.44-2.38, P < 0.01) were risk factors associated with PCF.
Correlation analysis indicated that serum CX3CL1 in COPD smokers was negatively correlated with FEV<sub>1</sub>/FVC (justified r = -0.319, P < 0.001), FEV<sub>1</sub>/Pre (justified r = -0.476, P < 0.001), FEV<sub>3</sub>/FVC (justified r = -0.354, P < 0.001), MMEF25-75/Pre (justified r = -0.428, P < 0.001), but positively correlated with CRP (justified r = 0.331, P < 0.001) and MMP-12 (justified r = 0.352, P < 0.001).
Correlation analysis indicated that serum CX3CL1 in COPD smokers was negatively correlated with FEV<sub>1</sub>/FVC (justified r = -0.319, P < 0.001), FEV<sub>1</sub>/Pre (justified r = -0.476, P < 0.001), FEV<sub>3</sub>/FVC (justified r = -0.354, P < 0.001), MMEF25-75/Pre (justified r = -0.428, P < 0.001), but positively correlated with CRP (justified r = 0.331, P < 0.001) and MMP-12 (justified r = 0.352, P < 0.001).
This is particularly important given recent completed and ongoing clinical trials with IL-1 biologics that have had varying degrees of failure and success as therapeutics for disease modification in asthma and COPD.
The following key points emerged from this analysis: 1) evidence is lacking on the comparison of short-acting vs. long-acting bronchodilators in patients with mild COPD; patients with moderate-to-severe COPD obtain greater benefit from long-acting bronchodilators; 2) the benefits of monotherapy with long-acting antimuscarinic agents (LAMA) and combined therapy with long-acting β<sub>2</sub>-agonists and inhaled corticosteroids (LABA/ICS) are similar, although the latter is associated with a greater risk of pneumonia; 3) LABA/LAMA offer greater benefits in terms of lung function and risk of exacerbation than LABA/ICS (the latter involve an increased risk of pneumonia), 4) LAMA/LABA/ICS have greater therapeutic benefits than LABA/LAMA on the risk of moderate-severe exacerbations.
Here we show that we can use an established transgenic animal model of COPD based on inducible IL13-driven pulmonary emphysema (IL13<sup>TG</sup>) to interrogate the mechanisms of skeletal muscle dysfunction.
This is particularly important given recent completed and ongoing clinical trials with IL-1 biologics that have had varying degrees of failure and success as therapeutics for disease modification in asthma and COPD.
Thus, whether a subgroup of COPD sufferers might respond to anti-IL-5 or other T2-directed biologics remains to be fully addressed and requires further investigation.
Recent evidence shows that increased HIF-1α expression can upregulate the platelet-activating factor receptor (PAFR) on the airway epithelial surface that is increased in smokers and particularly COPD patients.
Human bronchial epithelial cells were isolated from COPD (DHBE) bronchial tissues, co-cultured with IAV for 24 h, and were subsequently treated with SFJDC and/or oseltamivir.
The combination of visual and quantitative CT imaging features reflects different underlying pathological processes in the heterogeneous COPD syndrome and provides a useful approach to reclassify types of COPD.
Levels were higher in COPD patients [1.55 (0.45)g/L] and individuals with respiratory symptoms [1.57 (0.47)g/L] than in controls [1.43 (0.47)g/L], p<0.001, a finding which persisted after correction for age and CRP.
Single inhaler triple therapies providing an inhaled corticosteroid, a long-acting muscarinic antagonist, and a long-acting β<sub>2</sub>-agonist (ICS/LAMA/LABAs) are an emerging treatment option for chronic obstructive pulmonary disease (COPD).