作者: Derek W. Gilroy , Justine Newson , Prescilla Sawmynaden , Derek A. Willoughby , Jamie D. Croxtall
关键词: Phospholipase 、 Platelet-activating factor 、 Inflammation 、 Cyclooxygenase 、 Proinflammatory cytokine 、 Arachidonic acid 、 Immunology 、 Biology 、 Leukotriene B4 、 Phospholipase A2 、 Cell biology
摘要: Acute inflammation can be considered in terms of a series checkpoints where each phase cellular influx, persistence, and clearance is controlled by endogenous stop go signals. It becoming increasingly apparent that addition to initiating the inflammatory response, eicosanoids may also mediate resolution. This suggests there are two phases arachidonic acid release: one at onset for generation proinflammatory resolution synthesis proresolving eicosanoids. What unclear identity phospholipase (PLA2) isoforms involved this biphasic release acid. We show here type VI iPLA2 drives acute pleurisy through PGE2, LTB4, PAF, IL-1beta. However, during switch sequential induction first sPLA2 (types IIa V) mediates PAF lipoxin A4, which, turn, responsible subsequent IV cPLA2 prostaglandins. study its kind address respective roles PLA2 resolving identify as potentially selective target treatment diseases.