N-acetylcysteine decreases lung inflammation and fibrosis by modulating ROS and Nrf2 in mice model exposed to particulate matter.

Air pollutants can induce and incite airway diseases such as asthma. N-acetylcysteine (NAC) affects signaling pathways involved in apoptosis, angiogenesis, cell growth and arrest, redox-regulated gene expression, and the inflammatory response. However, it is not known how NAC change redox-regulated gene expression in asthma mouse model exposed to particulate matter (PM).

The Impact of Environmental Pollutants on Barrier Dysfunction in Respiratory Disease.

Respiratory epithelial cells form a selective barrier between the outside environment and underlying tissues. Epithelial cells are polarized and form specialized cell-cell junctions, known as the apical junctional complex (AJC). Assembly and disassembly of the AJC regulates epithelial morphogenesis and remodeling processes.

Effects of Air Pollutants on Airway Diseases.

Air pollutants include toxic particles and gases emitted in large quantities from many different combustible materials. They also include particulate matter (PM) and ozone, and biological contaminants, such as viruses and bacteria, which can penetrate the human airway and reach the bloodstream, triggering airway inflammation, dysfunction, and fibrosis. Pollutants that accumulate in the lungs exacerbate symptoms of respiratory diseases such as asthma and chronic obstructive pulmonary disease (COPD).

Titanium dioxide particles modulate epithelial barrier protein, Claudin 7 in asthma.

Epithelial barrier dysfunction is involved in allergic inflammation and asthma, due to increased exposure of sub-epithelial tissues to inhaled allergens and air pollutants. The tight junction proteins claudins (CLDNs) are important regulators of paracellular permeability. CLDN7 is expressed in the alveolar epithelium; however, its contribution to airway barrier function remains unclear.

Serum Calprotectin Is a Potential Marker in Patients with Asthma.

Background: Calprotectin is the major cytosolic protein in neutrophil granulocytes. Although asthma is known to cause eosinophilic inflammation, some patients with asthma have non-eosinophilic inflammation, which is characterized by local neutrophilic inflammation. The aim of this study was to assess calprotectin expression levels in a mouse model of asthma, and to observe the relationship of serum calprotectin level and clinical variables in patients with asthma.

Augmented angiogenic transcription factor, SOX18, is associated with asthma exacerbation.

Background: Asthma characterized by airway hyperresponsiveness, inflammation, fibrosis, and angiogenesis. SRY-related HMG-box 18 (SOX18) is an important transcription factor involved in angiogenesis, tissue injury, wound-healing, and in embryonic cardiovascular and lymphatic vessels development. The role of angiogenic transcription factors, SOX18 and the related, prospero homeobox 1 (PROX1) and chicken ovalbumin upstream promoter transcription factor II (COUP-TFII), in asthma has had limited study.