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Group IB Secretory Phospholipase A₂ Stimulates CXC Chemokine Ligand 8 Production via ERK and NF-B in Human Neutrophils¹

Eun Jin Jo^2,*,, Ha-Young Lee^2,*,, Youl-Nam Lee^*, Jung Im Kim^*,, Hyun-Kyu Kang^*, Dae-Won Park, Suk-Hwan Baek, Jong-Young Kwak^*, and Yoe-Sik Bae^3,*,

^* Medical Research Center for Cancer Molecular Therapy and Department of Biochemistry, College of Medicine, Dong-A University, Busan, Korea; and Department of Biochemistry and Molecular Biology, College of Medicine, Yeungnam University, Daegu, Korea

Although the level of group IB secretory phospholipase A₂ (sPLA₂-IB) has been reported to be up-regulated during inflammatory response, the role of sPLA₂-IB on the regulation of inflammation and immune responses has not been fully elucidated. In this study, we found that sPLA₂-IB stimulates the expression and secretion of CXCL8 without affecting other proinflammatory cytokines, such as IL-1 or TNF in human neutrophils. The induction of CXCL8 secretion by sPLA₂-IB occurs at both the transcription and translational levels and correlates with activation of NF-B. Moreover, the NF-B inhibitors pyrrolidinedithiocarbamate, dexamethasone, or sulfasalazine were found to prevent CXCL8 production by sPLA₂-IB in human neutrophils. In addition, the signaling events induced by sPLA₂-IB included activation of the MAPK ERK and an increase in intracellular Ca²⁺, which are both required for CXCL8 production. The exogenous addition of sPLA₂-IB did not induce arachidonic acid release from human neutrophils, and the inactivation of sPLA₂-IB by EGTA did not affect CXCL8 production by sPLA₂-IB in human neutrophils. Taken together, we suggest that sPLA₂-IB plays a role in the modulation of inflammatory and immune responses via the sPLA₂ receptor, by inducing CXCL8 in human neutrophils.

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