Перегляд вихідного коду сторінки A Neutral Glimpse At DDR1

These treated cells also showed upregulation of Streptococcus pneumoniae adhesion. Bacterial wall phosphorylcholine [http://www.selleckchem.com/products/Methazolastone.html Temozolomide purchase] specifically binds to PAFr expressed on airway epithelium, so facilitating adherence and tissue invasion, which may be relevant to COPD. Moreover, the use of inhaled corticosteroids (ICS) in COPD patients is associated with an increased risk of invasive respiratory pneumococcal infections. In this study we have investigated whether PAFr expression is especially upregulated in airway epithelium in COPD patients and whether this expression may be modulated by ICS therapy. Methods:?Cross-sectionally we evaluated PAFr expression in bronchial biopsies from 15 COPD patients who were current smokers (COPD-CS), 12 COPD ex-smokers (COPD-ES), compared to biopsies from 16 smokers with normal lung function (NLFS). We assessed immunostaining with anti-PAFr monoclonal antibody. We also used material from a previous double-blinded, randomized, placebo-controlled 6 months ICS intervention study in COPD patients to explore the effect of ICS on PAFr expression. We employed computer-aided image analysis to quantify the percentage of epithelium stained for PAFr. Results:?Markedly enhanced expression of PAFr was found in both COPD-CS (p?[http://www.selleckchem.com/products/ABT-888.html Veliparib solubility dmso] 6 months. Conclusion:?Epithelial PAFr expression is upregulated in smokers but especially in COPD, but not obviously affected by ICS therapy. Key words:?airway epithelium, inhaled corticosteroids, platelet activating factor receptor, pneumococcal infections. VLAHOS R, SEOW H, BOZINOVSKI S, HAMILTON J, ANDERSON G The University of Melbourne Introduction:?Exacerbations of COPD account for significant morbidity and mortality [http://en.wikipedia.org/wiki/DDR1 DDR1] and are a major economic burden to society. Influenza virus infections are a common cause of COPD exacerbations. Current anti-inflammatory agents (i.e. corticosteroids) are often not very effective at preventing and/or treating infection-induced COPD, highlighting the need for new therapeutic strategies. We have previously shown that neutralizing GM-CSF in vivo reduces LPS- and cigarette smoke (CS)-induced lung inflammation. Aim:?To investigate the role of GM-CSF in an animal model of COPD exacerbations induced by influenza A virus. Methods:?Male Balb/C mice were exposed to CS generated from 9 cigarettes per day for 4 days. On day 5, mice were infected with influenza (flu) A (Mem71, H3N1, 1?��?104.5 PFU). Mice were treated with 22E9 (anti-GM-CSF mAb) and isotype control antibody (100?��g/mouse, in) 3?h before infection. BALF inflammation, viral titre, and whole lung cytokine, chemokine and protease mRNA expression were assessed 3 and 5 days post infection.