Abstract

In this study, we observed that lysophosphatidylglycerol (LPG) completely inhibited a formyl peptide receptor like-1 (FPRL1) agonist (MMK-1)-stimulated chemotactic migration in human phagocytes, such as neutrophils and monocytes. LPG also dramatically inhibited IL-1beta production by another FPRL1 agonist serum amyloid A (SAA) in human phagocytes. However, LPG itself induced intracellular calcium increase and superoxide anion production in human phagocytes. Keeping in mind that phagocytes migration and IL-1beta production by FPRL1 are important for the induction of inflammatory response, our data suggest that LPG can be regarded as a useful material for the modulation of inflammatory response induced by FPRL1 activation.

Highlights

  • Formyl peptide receptor like-1 (FPRL1) is one of the classic chemoattractant receptors and is made up of a seven trans-membrane-spanning G proteincoupled receptor (Le et al, 2001, 2002)

  • Since phagocytes recruitment into infected or inflammatory site is crucial for the induction of innate immune response, and MMK-1 and its specific receptor (FPRL1) have been reported to play a key role in the regulation of phagocyte recruiting, it has been important issue to identify certain molecules that modulate MMK-1 and FPRL1-mediated cellular response

  • We demonstrated that LPG inhibited MMK-1-stimulated chemotactic migration in human neutrophils and monocytes

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Summary

Introduction

Formyl peptide receptor like-1 (FPRL1) is one of the classic chemoattractant receptors and is made up of a seven trans-membrane-spanning G proteincoupled receptor (Le et al, 2001, 2002). FPRL1 is highly expressed on phagocytic cells such as neutrophils, monocytes, and dendritic cells (Le et al, 2001, 2002). In terms of functional activity of FPRL1, it has been found to mediate the chemotactic migration of phagocytes in a pertussis toxin (PTX)-sensitive manner, indicating the receptor couple to the Gi subfamily of G proteins (Le et al, 2001, 2002). FPRL1 plays an important role in immunological function, including host defenses against pathogen infection (Le et al, 2001, 2002).

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