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Induction of CCR2-dependent macrophage accumulation by oxidized phospholipids in the air-pouch model of inflammation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Kadl, Alexandra Galkina, Elena Leitinger, Norbert
Description	Country affiliation: United States Author Affiliation: Kadl A ( Robert M. Berne Cardiovascular Research Center, University of Virginia, Charlottesville, VA 22908, USA.)
Abstract	OBJECTIVE: Macrophages are key players in the pathogenesis of rheumatoid synovitis as well as in atherosclerosis. To determine whether atherogenic oxidized phospholipids potentially contribute to synovial inflammation and subsequent monocyte/macrophage recruitment, we examined the effects of oxidized 1- palmitoyl-2-arachidonoyl-sn-3-glycero-phosphorylcholine (OxPAPC) on chemokine expression and leukocyte recruitment in a facsimile synovium in vivo using the murine air-pouch model. METHODS: Air pouches were raised by 2 injections of sterile air, and inflammation was induced by injecting either lipopolysaccharide (LPS) or OxPAPC into the pouch lumen. Inflammation was assessed by analysis of inflammatory gene expression using reverse transcription-polymerase chain reaction or immunohistochemical analysis, and leukocytes were quantified in the lavage fluid and in the pouch wall after staining with Giemsa or after enzymatic digestion followed by fluorescence-activated cell sorter analysis. RESULTS: Application of OxPAPC resulted in selective recruitment of monocyte/macrophages into the air-pouch wall, but not in the lumen. In contrast, LPS induced both monocyte and neutrophil accumulation in the pouch lumen as well as in the wall. LPS, but not OxPAPC, induced the expression of adhesion molecules E-selectin, P-selectin, intercellular adhesion molecule 1, and vascular cell adhesion molecule 1. OxPAPC increased the expression of the CCR2 ligands monocyte chemotactic protein 1 (MCP-1), MCP-3, and MCP-5, as well as RANTES and growth-related oncogene alpha (GROalpha), while it down-regulated the expression of CCR2 on macrophages. Moreover, oxidized phospholipid-induced macrophage accumulation was abrogated in CCR2-/- mice. CONCLUSION: These data demonstrate that oxidized phospholipids trigger a type of inflammatory response that leads to selective macrophage accumulation in vivo, a process relevant for the pathogenesis of chronic inflammatory rheumatic diseases.
File Format	HTM / HTML
ISSN	00043591
e-ISSN	15290131
DOI	10.1002/art.24448
Journal	Arthritis & Rheumatism
Issue Number	5
Volume Number	60
Language	English
Publisher	Wiley-Blackwell
Publisher Date	2009-05-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Phosphatidylcholines Macrophages Lipopolysaccharides Histological Techniques Physiology Carboxypeptidases A Synovial Membrane Rheumatic Diseases Vascular Cell Adhesion Molecule-1 Chemokine Ccl5 Mice, Inbred C57bl Neutrophils Chemokine Cxcl1 Intercellular Adhesion Molecule-1 Inflammation Pharmacology Physiopathology Monocyte Chemoattractant Proteins E-selectin Monocytes Animals Mice Chemokine Ccl2 Receptors, Ccr2 P-selectin Discipline Rheumatic Diseases
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology Pharmacology (medical) Rheumatology

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