American journal of respiratory and critical care medicine
-
Whether allergic airway inflammation mediates the association between overweight or obesity and childhood asthma is unknown. ⋯ Adiposity indicators are associated with asthma in children with low FeNO. Among children with asthma, adiposity indicators are associated with worse asthma severity or control in those with high FeNO.
-
Am. J. Respir. Crit. Care Med. · Jul 2014
T regulatory cells and PD-1+ T cells contribute to effector T cell dysfunction in COPD patients.
Previous studies from our laboratory have shown that peripheral blood mononuclear cells (PBMCs) from patients with chronic obstructive pulmonary disease (COPD) prone to exacerbations with nontypeable Haemophilus influenzae have impaired responses to lipoprotein P6. We hypothesized that an underlying immunosuppressive network could be responsible for the defective antibacterial immunity observed in these patients. We evaluated T regulatory cells (Tregs), myeloid-derived suppressor cells (MDSC), and exhausted T effector cells (programmed death 1 [PD-1](+)) in patients with COPD, because these cells are known to play a pivotal role in suppressing immune responses. ⋯ Functionally suppressive Tregs, MDSCs, and exhausted PD-1(+) T cells contribute to effector T-cell dysfunction in COPD.
-
Am. J. Respir. Crit. Care Med. · Jul 2014
STudy of Active Duty Military for Pulmonary Disease Related to Environmental Deployment Exposures (STAMPEDE).
Because of increased levels of airborne particulate matter in Southwest Asia, deployed military personnel are at risk for developing acute and chronic lung diseases. Increased respiratory symptoms are reported, but limited data exist on reported lung diseases. ⋯ Evaluation of new respiratory symptoms in military personnel after service in Southwest Asia should focus on airway hyperreactivity from exposures to higher levels of ambient particulate matter. These patients may be difficult to diagnose and require close follow-up.
-
Am. J. Respir. Crit. Care Med. · Jul 2014
Dysregulation of Claudin-5 in HIV-induced Interstitial Pneumonitis and Lung Vascular Injury: Protective Role of PPAR-γ
HIV-1-induced interstitial pneumonitis (IP) is a serious complication of HIV-1 infection, characterized by inflammation and cellular infiltration in lungs, often leading to respiratory failure and death. The barrier function of the pulmonary endothelium is caused in part by tight junction (TJ) proteins, such as claudin-5. Peroxisome proliferator-activated receptor (PPAR)-γ is expressed in lung tissues and regulates inflammation. We hypothesize that HIV-1 induces vascular lung injury, and HIV-1-mediated damage of the pulmonary endothelium and IP is associated with dysregulation of PPAR-γ. ⋯ HIV-induced IP is associated with injury to the lung vascular endothelium, with decreased TJ and PPAR-γ expression, and increased pulmonary macrophage infiltration. PPAR-γ ligands abrogated these effects. Thus, regulation of PPAR-γ can be a therapeutic approach against HIV-1-induced vascular damage and IP in infected humans. Removal of Expression of Concern: Issues leading to the previous expression of concern for this article have been resolved after further revisions and editorial review. No further concerns exist.