AI Article Synopsis
- Allergens, viral, and bacterial infections contribute to asthma exacerbations by worsening airway inflammation, where cPLA2 α and sPLA2X play crucial roles in producing eicosanoids from arachidonic acid.
- A study examined how rDer p1, rFel d1, and lipopolysaccharide influence cPLA2 α expression and sPLA2X secretion in asthmatic individuals' PBMCs and A549 cells, revealing changes in enzyme activity.
- The findings indicate that sPLA2X is significantly released in asthmatics compared to healthy individuals, with rDer p1 promoting more sPLA2X secretion, while rFel d1 decreases cPLA2 α expression, highlighting the role of these enzymes in
Article Abstract
Allergens, viral, and bacterial infections are responsible for asthma exacerbations that occur with progression of airway inflammation. cPLA2 α and sPLA2X are responsible for delivery of arachidonic acid for production of eicosanoids-one of the key mediators of airway inflammation. However, cPLA2 α 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 cPLA2 α 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 cPLA2 α 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 cPLA2 α protein expression. rFel d1 caused decrease in cPLA2 α relative expression in PBMC of asthmatics and in A549 cells. Summarizing, Der p1 and Fel d1 involve phospholipase A2 enzymes in their action. sPLA2X seems to be one of important PLA2 isoform in allergic inflammation, especially caused by house dust mite allergens.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4163415 | PMC |
| http://dx.doi.org/10.1155/2014/670814 | DOI Listing |
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