Human rhinovirus proteinase 2A induces TH1 and TH2 immunity in patients with chronic obstructive pulmonary disease.

BACKGROUND: Tobacco-related lung diseases, including chronic obstructive pulmonary disease (COPD), are major causes of lung-related disability and death worldwide. Acute exacerbation of COPD (AE-COPD) is commonly associated with upper and lower respiratory tract viral infections and can result in respiratory failure in those with advanced lung disease. OBJECTIVE: We sought to determine the mechanism underlying COPD exacerbation and host response to pathogen-derived factors. METHODS: Over a 24-month period, we assessed the viral causes for upper and lower respiratory tract infections in patients with COPD (n = 155) and control subjects (n = 103). We collected nasal and bronchoalveolar lavage fluid and peripheral blood under baseline and exacerbated conditions. We determined the effect of human rhinovirus (HRV) proteinases on T-cell activation in human subjects and mice. RESULTS: HRVs are isolated from nasal and lung fluid from subjects with AE-COPD. Bronchoalveolar lavage fluid and CD4 T cells from patients with COPD exhibited a T(H)1 and T(H)2 cell cytokine phenotype during acute infection. HRV-encoded proteinase 2A activated monocyte-derived dendritic cells in vitro and induced strong T(H)1 and T(H)2 immune responses from CD4 T cells. Intranasal administration of recombinant rhinovirus proteinase 2A in mice resulted in an increase in airway hyperreactivity, lung inflammation, and IL-4 and IFN-gamma production from CD4 T cells. CONCLUSION: Our findings suggest that patients with severe COPD show T(H)1- and T(H)2-biased responses during AE-COPD. HRV-encoded proteinase 2A, like other microbial proteinases, could provide a T(H)1- and T(H)2-biasing adjuvant factor during upper and lower respiratory tract infection in patients with severe COPD. Alteration of the immune response to secreted viral proteinases might contribute to worsening of dyspnea and respiratory failure in patients with COPD.

An inventory of trees in Dublin city centre.

While urban areas are often considered to be comprised chiefly of artificial surfaces, they can contain a substantial portion of green space and a great diversity of natural habitats. These spaces include public parks, private gardens and street trees, all of which can provide valuable environmental services, such as improved air quality. Trees play a particular role in cities as they are often placed along roadsides and in the median strip of busy streets. As such they regulate access to sunshine, restrict airflow, provide shelter, scavenge air pollutants and manage noise at the street level. A tree planting policy can be an important part of a broader environmental strategy aimed at improving the quality of life in urban areas but this requires up-to-date knowledge of the current tree stock, which does not exist for Dublin. This article presents an inventory of trees in Dublin's city centre, defined as the area between the Grand and Royal canals. The results show that there are over 10,000 trees in the study area representing a density of 684 trees km-2 or one tree to approximately every 50 residents of the city centre. The tree canopy extent when in full foliage was nearly 1 km2 in extent or 6% of the study area. A more detailed analysis of those trees planted along streets shows little species variation but clear distinction in the sizes of trees, which is indicative of the age of planting. These data are used to estimate the carbon stored in Dublin's trees.

Cross-sectional analysis of the utility of pulmonary function tests in predicting emphysema in ever-smokers.

Emphysema is largely an under-diagnosed medical condition that can exist in smokers in the absence of airway obstruction. We aimed to determine the sensitivity and specificity of pulmonary function tests (PFTs) in assessing emphysema using quantitative CT scans as the reference standard. We enrolled 224 ever-smokers (current or former) over the age of 40. CT of thorax was used to quantify the low attenuation area (% emphysema), and to measure the standardized airway wall thickness. PFTs were used individually and in combination to predict their ability to discriminate radiographic emphysema. Significant emphysema (>7%) was detected in 122 (54%) subjects. Twenty six (21%) emphysema subjects had no evidence of airflow obstruction (FEV(1)/FVC ratio <70%), while all subjects with >23% emphysema showed airflow obstruction. The sensitivity and specificity of spirometry for detecting radiographic emphysema were 79% and 75%, respectively. Standardized airway wall thickness was increased in subjects with airflow obstruction, but did not correlate with emphysema severity. In this cohort of lifetime ever-smokers, PFTs alone were inadequate for diagnosing emphysema. Airway wall thickness quantified by CT morphometry was associated with airflow limitation, but not with emphysema indicating that the heterogeneous nature of lung disease in smokers may represent distinct phenotypes.