Coordinate Regulation of Toll-like Receptor-mediated Arachidonic Acid Mobilization in Macrophages by Group IVA and Group V Phospholipase A2s

نویسندگان

  • Violeta Ruipérez
  • Alma M. Astudillo
  • María A. Balboa
  • Jesús Balsinde
چکیده

Macrophages can be activated through Toll-like receptors (TLR) for a variety of innate immune responses. In contrast with the wealth of data existing on TLRdependent gene expression and resultant cytokine production, very little is known on the mechanisms governing TLR-mediated arachidonic acid (AA) mobilization and subsequent eicosanoid production. We have previously reported the involvement of both cytosolic group IVA phospholipase A2 (cPLA2) and secreted group V phospholipase A2 (sPLA2-V) in regulating the AA mobilization response of macrophages exposed to bacterial lipopolysaccharide, a TLR4 agonist. In the present study, we have used multiple TLR agonists to define the role of various PLA2s in macrophage AA release via TLRs. Activation of P388D1 and RAW2647.1 macrophage-like cells via TLR1/2, TLR2, TLR3, TLR4, TLR6/2 and TLR7, but not TLR5 or TLR9, resulted in AA mobilization that appears to involve the activation of both cPLA2 and sPLA2 but not of calcium-independent phospholipase A2. Furthermore, inhibition of sPLA2-V by RNA interference or by two cell-permeable compounds, namely scalaradial and manoalide, resulted in a marked reduction of the phosphorylation of ERK1/2 and cPLA2 via TLR1/2, TLR2, TLR3 and TLR4, leading to attenuated AA mobilization. Collectively, the results suggest a model whereby sPLA2V contributes to the macrophage AA mobilization response via various TLRs by amplifying cPLA2 activation through the ERK1/2 phosphorylation cascade.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Cytosolic group IVA and calcium-independent group VIA phospholipase A2s act on distinct phospholipid pools in zymosan-stimulated mouse peritoneal macrophages.

Phospholipase A2s generate lipid mediators that constitute an important component of the integrated response of macrophages to stimuli of the innate immune response. Because these cells contain multiple phospholipase A2 forms, the challenge is to elucidate the roles that each of these forms plays in regulating normal cellular processes and in disease pathogenesis. A major issue is to precisely ...

متن کامل

Up-regulation of TLR2 and TLR4 in high mobility group Box1-stimulated macrophages in pulpitis patients

Objective(s): High Mobility Group Box1 (HMGB1) is a nonhistone, DNA-binding protein that serves a crucial role in regulating gene transcription and is involved in a variety of proinflammatory, extracellular activities. The aim of this study was to explore whether HMGB1 stimulation can up-regulate the expression of Toll-like Receptor 2 (TLR2) and Toll-like Receptor 4 (TLR4) on macrophages from p...

متن کامل

The Cationic Cluster of Group IVA Phospholipase A2 (Lys/Lys/Lys/Lys) Is Involved in Translocation of the Enzyme to Phagosomes in Human Macrophages

Group IVA cytosolic phospholipase A2α (cPLA2α) plays a role in the microbicidal machinery of immune cells by translocating to phagosomes to initiate the production of antimicrobial eicosanoids. In the present work we have studied the involvement of the cationic cluster of cPLA2α (Lys/Lys/Lys/Lys) in the translocation of cPLA2α to the phagosomal cup in human macrophages responding to opsonized z...

متن کامل

Oxidative stress and arachidonic acid mobilization.

Reactive oxygen species are known to contribute to tissue damage during injury and inflammation. However, these species can also be sensed by the cells and trigger intracellular signaling cascades. This review examines recent evidence on the involvement of reactive oxygen species in lipid signaling. Attention is focused on activation of phospholipase A2s, enzymes whose action on membrane phosph...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2009