The Step Further to Understand the Role of Cytosolic Phospholipase A2Alpha and Group X Secretory Phospholipase A2in Allergic Inflammation: Pilot Study

Abstract

Allergens, viral, and bacterial infections are responsible for asthma exacerbations that occur with progression of airway inflammation. cPLA2α and sPLA2X are responsible for delivery of arachidonic acid for production of eicosanoids—one of the key mediators of airway inflammation. However, cPLA2α and sPLA2X role in allergic inflammation has not been fully elucidated. The aim of this study was to analyze the influence of rDer p1 and rFel d1 and lipopolysaccharide (LPS) on cPLA2α expression and sPLA2X secretion in PBMC of asthmatics and in A549 cell line. PBMC isolated from 14 subjects, as well as A549 cells, were stimulated with rDer p1, rFel d1, and LPS. Immunoblotting technique was used to study the changes in cPLA2α protein expression and ELISA was used to analyze the release of sPLA2X. PBMC of asthmatics released more sPLA2X than those from healthy controls in the steady state. rDer p1 induced more sPLA2X secretion than cPLA2α protein expression. rFel d1 caused decrease in cPLA2α relative expression in PBMC of asthmatics and in A549 cells. Summarizing, Der p1 and Fel d1 involve phospholipase A2enzymes in their action. sPLA2X seems to be one of important PLA2isoform in allergic inflammation, especially caused by house dust mite allergens.