If a patient has a genetic defect causing continuously elevated cytosolic phospholipase A2 (cPLA2) activity, which consequence is most likely within inflammatory cells?

💡 Explanation

Sustained cPLA2 activation increases arachidonic acid release from membrane phospholipids, because this is the substrate for prostaglandin synthesis via cyclooxygenase (COX) enzymes; therefore, prostaglandin synthesis will dominate, rather than leukotriene production which uses a different substrate pathway, or impacts on TNF-alpha or NF-kB.

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