Peroxisome proliferator-activated receptor-gamma agonists inhibit respiratory syncytial virus-induced expression of intercellular adhesion molecule-1 in human lung epithelial cells.

Respiratory syncytial virus (RSV) is the major causative agent of severe lower respiratory tract disease and death in infants worldwide. The epithelial cells of the airways are the target cells for RSV infection and the site of the majority of the inflammation associated with the disease. However, despite five decades of intensive RSV research there exist neither an effective active vaccine nor a promising antiviral and anti-inflammatory therapy.

Peroxisome proliferator-activated receptor-gamma agonists inhibit the replication of respiratory syncytial virus (RSV) in human lung epithelial cells.

We have previously shown that peroxisome proliferator-activated receptor-gamma (PPARgamma) agonists inhibited the inflammatory response of RSV-infected human lung epithelial cells. In this study, we supply evidence that specific PPARgamma agonists (15d-PGJ2, ciglitazone, troglitazone, Fmoc-Leu) efficiently blocked the RSV-induced cytotoxicity and development of syncytia in tissue culture (A549, HEp-2). All PPARgamma agonists under study markedly inhibited the cell surface expression of the viral G and F protein on RSV-infected A549 cells.

Peroxisome-proliferator-activated receptor-gamma agonists inhibit the release of proinflammatory cytokines from RSV-infected epithelial cells.

The epithelial cells of the airways are the target cells for respiratory syncytial virus (RSV) infection and the site of the majority of the inflammation associated with the disease. Recently, peroxisome-proliferator-activated receptor gamma (PPARgamma), a member of the nuclear hormone receptor superfamily, has been shown to possess anti-inflammatory properties. Therefore, we investigated the role of PPARgamma agonists (15d-PGJ(2), ciglitazone and troglitazone) on the synthesis of RSV-induced cytokine release from RSV-infected human lung epithelial cells (A549).

Area-coded effective medium structures, a new type of grating design.

We propose a new way to design gratings with desired diffraction properties by using subwavelength feature sizes perpendicular to the ordinary superwavelength grating period. This is different from well-known one-dimensional binary-blazed gratings that use a structuring along the grating period and thus opens new flexibility in generating arbitrary effective-index distributions in the direction of the grating period. Since the subwavelength features form contiguous areas, they are called area-coded effective medium structures (ACES).

Respiratory syncytial virus infection of human lung endothelial cells enhances selectively intercellular adhesion molecule-1 expression.

Respiratory syncytial virus (RSV) is worldwide the most frequent cause of bronchiolitis and pneumonia in infants requiring hospitalization. In the present study, we supply evidence that human lung microvascular endothelial cells, human pulmonary lung aorta endothelial cells, and HUVEC are target cells for productive RSV infection. All three RSV-infected endothelial cell types showed an enhanced cell surface expression of ICAM-1 (CD54), which increased in a time- and RSV-dose-dependent manner.

Respiratory syncytial virus deficient in soluble G protein induced an increased proinflammatory response in human lung epithelial cells.

Respiratory syncytial virus (RSV) is worldwide the single most important respiratory pathogen in infancy and early childhood. The G glycoprotein of RSV, named attachment protein, is produced by RSV-infected lung epithelial cells in both a membrane-anchored (mG protein) and a soluble form (sG protein) that is secreted by the epithelial cell. Currently, the biological role of the sG protein in primary RSV infection is still elusive.

Prospective study of human metapneumovirus infection in children less than 3 years of age.

Most lower respiratory tract infections (LRTIs) in children under the age of 3 years are due to respiratory syncytial virus (RSV). Epidemiological, host, and viral factors eventually account for the severity of LRTIs, but they do not completely explain it. Human metapneumovirus (hMPV) was recently identified in children with LRTIs.