IL-4Rα blockade reduces influenza-associated morbidity in a murine model of allergic asthma.

Background: Asthma was identified as the most common comorbidity in hospitalized patients during the 2009 H1N1 influenza pandemic. We determined using a murine model of allergic asthma whether these mice experienced increased morbidity from pandemic H1N1 (pH1N1) viral infection and whether blockade of interleukin-4 receptor α (IL-4Rα), a critical mediator of T2 signalling, improved their outcomes.

Methods: Male BALB/c mice were intranasally sensitized with house dust mite antigen (Der p 1) for 2 weeks; the mice were then inoculated intranasally with a single dose of pandemic H1N1 (pH1N1).

Adhesion molecule gene variants and plasma protein levels in patients with suspected obstructive sleep apnea.

Study Objectives: Untreated obstructive sleep apnea (OSA) patients have an increased risk of cardiovascular disease (CVD). Adhesion molecules, including soluble E-selectin (sE-selectin), intercellular adhesion molecule-1 (ICAM-1), and vascular adhesion molecule-1 (VCAM-1), are associated with incident CVD. We hypothesized that specific genetic variants will be associated with plasma levels of adhesion molecules in suspected OSA patients.

The role of beta-blockers in the management of chronic obstructive pulmonary disease.

The use of beta-blockers in chronic obstructive pulmonary disease (COPD) is controversial, primarily due to concerns that they may worsen lung function and attenuate bronchodilator response. Areas covered: This review summarizes the reasons for and against the use of beta-blockers in COPD by evaluating the literature on the effects of these drugs on lung function, exacerbation rate, and mortality. The safety of beta-blockers in COPD patients with concomitant heart failure, an entity that is not always distinguishable from COPD exacerbations, is also explored.

Lung exposure to lipopolysaccharide causes atherosclerotic plaque destabilisation.

Epidemiological studies have implicated lung inflammation as a risk factor for acute cardiovascular events, but the underlying mechanisms linking lung injury with cardiovascular events are largely unknown.Our objective was to develop a novel murine model of acute atheromatous plaque rupture related to lung inflammation and to investigate the role of neutrophils in this process.Lipopolysaccharide (LPS; 3 mg·kg(-1)) or saline (control) was instilled directly into the lungs of male apolipoprotein E-null C57BL/6J mice following 8 weeks of a Western-type diet.

Current methods to diagnose small airway disease in patients with COPD.

The small airways are characterized by an internal diameter < 2 mm and absence of cartilage. Approximately 10-25% of total airway resistance in healthy lungs is due to the small airways, with their contribution to total airway resistance increasing substantially in chronic obstructive pulmonary disease (COPD). As the small airways are located in the lung periphery, they are not easily evaluable, which can potentially interfere with the diagnosis (especially at early stages), monitoring, detection of responses to clinical interventions, and prognostic evaluation in COPD.

Absolute leukocyte telomere length in HIV-infected and uninfected individuals: evidence of accelerated cell senescence in HIV-associated chronic obstructive pulmonary disease.

Combination antiretroviral therapy (cART) has extended the longevity of human immunodeficiency virus (HIV)-infected individuals. However, this has resulted in greater awareness of age-associated diseases such as chronic obstructive pulmonary disease (COPD). Accelerated cellular senescence may be responsible, but its magnitude as measured by leukocyte telomere length is unknown and its relationship to HIV-associated COPD has not yet been established.

Plasma sCD14 as a biomarker to predict pulmonary exacerbations in cystic fibrosis.

Background: One in four cystic fibrosis (CF) patients diagnosed with a pulmonary exacerbation will not recover their baseline lung function despite standard treatment. This highlights the importance of preventing such events. Clinical decision-making can be improved through a simple blood test that predicts individuals at elevated short-term risk of an exacerbation.

A possible role for CD8+ and non-CD8+ cell granzyme B in early small airway wall remodelling in centrilobular emphysema.

Background And Objective: CD8(+) cell infiltration and apoptosis of airway epithelial cells are increased in chronic obstructive pulmonary disease (COPD). CD8(+) T cells induce apoptosis by releasing granzymes, which can also cause extracellular matrix degradation and remodelling. Granzyme B levels and T cells expressing granzyme B are increased in bronchoalveolar lavage fluid of COPD patients, which suggests that granzyme B may contribute to the pathogenesis of COPD.

The relationship of systemic inflammation to prior hospitalization in adult patients with cystic fibrosis.

Background: In cystic fibrosis (CF) patients, it has been suggested that systemic inflammation may be an important risk factor for poor health outcomes. The relationship of plasma inflammatory biomarkers to lung function and hospitalization history remains largely unexplored.

Methods: This cross-sectional study included 58 consecutive, clinically stable adults from the CF Clinic at St.

The possible role of granzyme B in the pathogenesis of chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is a highly prevalent inflammatory lung condition characterized by airways disease and emphysema, and the precise mechanism of pathogenesis is poorly understood. The consistent features of COPD include protease-antiprotease imbalance, inflammation and accelerated aging caused by apoptosis or senescence. One family of molecules involved in all of these processes is the granzymes, serine proteases with the best-known member being granzyme B (GzmB).