The Step Further to Understand the Role of Cytosolic Phospholipase A(2) Alpha and Group X Secretory Phospholipase A(2) in Allergic Inflammation: Pilot Study

Allergens, viral, and bacterial infections are responsible for asthma exacerbations that occur with progression of airway inflammation. cPLA(2) α and sPLA(2)X are responsible for delivery of arachidonic acid for production of eicosanoids—one of the key mediators of airway inflammation. However, cPLA(2) α and sPLA(2)X 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 cPLA(2) α expression and sPLA(2)X 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 cPLA(2) α protein expression and ELISA was used to analyze the release of sPLA(2)X. PBMC of asthmatics released more sPLA(2)X than those from healthy controls in the steady state. rDer p1 induced more sPLA(2)X secretion than cPLA(2) α protein expression. rFel d1 caused decrease in cPLA(2) α relative expression in PBMC of asthmatics and in A549 cells. Summarizing, Der p1 and Fel d1 involve phospholipase A(2) enzymes in their action. sPLA(2)X seems to be one of important PLA(2) isoform in allergic inflammation, especially caused by house dust mite allergens.