Interleukin-8 Production by Macrophages From Atheromatous Plaques

Apostolopoulos, Jim; Davenport, Piers; Tipping, Peter G.

doi:10.1161/01.atv.16.8.1007

Cited by 142 publications

(93 citation statements)

References 21 publications

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“…Human atheroma contain various chemokines including MCP-1, IL-8, MIP-1␤, IP-10, and RANTES (23)(24)(25)(26). Targeted disruption of the gene for MCP-1, its receptor CCR-2, or the murine homologue of IL-8 receptor, CXCR-2, significantly decreased atherogenesis in mice (27)(28)(29).…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin E2 Suppresses Chemokine Production in Human Macrophages through the EP4 Receptor

Takayama¹,

García‐Cardeña

Sukhova³

et al. 2002

Journal of Biological Chemistry

310

272

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Pro-inflammatory pathways participate in the pathogenesis of atherosclerosis. However, the role of endogenous anti-inflammatory pathways in atheroma has received much less attention. Therefore, using cDNA microarrays, we screened for genes regulated by prostaglandin E 2 (PGE 2 ), a potential endogenous anti-inflammatory mediator, in lipopolysaccharide (LPS)-treated human macrophages (M⌽). PGE 2 (50 nM) attenuated LPS-induced mRNA and protein expression of chemokines including monocyte chemoattractant protein-1, interleukin-8, macrophage inflammatory protein-1␣ and -1␤, and interferon-inducible protein-10. PGE 2 also inhibited the tumor necrosis factor-␣-, interferon-␥-, and interleukin-1␤-mediated expression of these chemokines. In contrast to the case of M⌽, PGE 2 did not suppress chemokine expression in human endothelial and smooth muscle cells (SMC) treated with LPS and pro-inflammatory cytokines. To assess the potential paracrine effect of endogenous PGE 2 on macrophagederived chemokine production, we co-cultured M⌽ with SMC in the presence of LPS. In these co-cultures, cyclooxygenase-2-dependent PGE 2 production exceeded that in the mono-cultures, and MIP-1␤ declined significantly compared with M⌽ cultured without SMC. We further documented prominent expression of the PGE 2 receptor EP4 in M⌽ in both culture and human atheroma. Moreover, a selective EP4 antagonist completely reversed PGE 2 -mediated suppression of chemokine production. Thus, endogenous PGE 2 may modulate inflammation during atherogenesis and other inflammatory diseases by suppressing macrophage-derived chemokine production via the EP4 receptor.

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Section: Discussionmentioning

confidence: 99%

Prostaglandin E2 Suppresses Chemokine Production in Human Macrophages through the EP4 Receptor

Takayama¹,

García‐Cardeña

Sukhova³

et al. 2002

Journal of Biological Chemistry

310

272

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“…It has been demonstrated that MCP-1 is synthesized in inflamed gingiva by vascular endothelial cells and mononuclear phagocytes [12]. Apostolopoulos et al [13] found IL-8 mRNA in carotid plaque, and Moreau et al [14] showed that IL-8 played a potential role in atherogenesis by inhibiting tissue inhibitors of metalloproteinase-1 expression. MCP-1 has been suggested to induce macrophage infiltration into the arterial wall [15].…”

Section: Introductionmentioning

confidence: 99%

Treponema denticola induces interleukin-8 and macrophage chemoattractant protein 1 production in human umbilical vein epithelial cells

Okuda

Kimizuka

Miyamoto

et al. 2007

Microbes and Infection

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Treponema denticola, a major pathogen of periodontitis, has also been detected in the lesions of atherosclerosis. The aim of this study was to investigate induction of chemokine production in human umbilical vein endothelial cells (HUVECs) by T. denticola and determine whether those chemokines were degraded by a protease, dentilisin. T. denticola ATCC35405 or dentilisin-deficient mutant K1 were added to HUVECs and levels of interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) in the culture supernatants were determined by enzyme-linked immunosorbent assay. T. denticola ATCC35405 induced production of IL-8 in a time-dependent manner, with both production of IL-8 and expression of IL-8 mRNA showing higher levels than with exposure to dentilisin-deficient mutant K1. Although exposure to ATCC35405 induced expression of MCP-1 mRNA in the HUVECs, MCP-1 levels were remained similar to that in unstimulated cells. IL-8 and MCP-1 showed partial hydrolysis with exposure to T. denticola ATCC35405, but not with T. denticola K1. These results suggest that T. denticola can evade host defense mechanisms by modulating production of IL-8 and MCP-1, and that this play a role in the development of chronic infections such as periodontitis. The association of T. denticola infection to atherosclerosis was also discussed based on the present study.-3 -

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“…[27][28][29][30] Furthermore, peripheral blood mononuclear cells from hypercholesterolemic patients have a marked enhancement of IL-8 production. 31 Mice do not express a peptide homologue of IL-8, but they do express one of the GRO chemokines, KC/GRO-␣, in the intima of advanced atherosclerotic lesions in the chimeric LDLR Ϫ/Ϫ mice.…”

mentioning

confidence: 99%

Up-Regulated Expression of the CXCR2 Ligand KC/GRO-α in Atherosclerotic Lesions Plays a Central Role in Macrophage Accumulation and Lesion Progression

Boisvert

Rose

Johnson

et al. 2006

The American Journal of Pathology

172

120

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Macrophage-mediated inflammation is central to atherogenesis. We have determined previously that the CXC chemokine receptor CXCR2 is involved in advanced atherosclerosis. We sought to determine whether one of the ligands of CXCR2, KC/GRO-␣, can also modulate atherogenesis. KC/GRO-␣ ؊/؊ mice were generated and mated with the atherosclerosis-prone LDLR ؊/؊ mice. There was a significant reduction in atherosclerosis in mice lacking KC/GRO-␣; however, this reduction was only approximately half that seen previously in mice lacking CXCR2 in the leukocyte. To determine whether CXCR2 is involved in the early formation of atherosclerosis, leukocyte-specific CXCR2 ؊/؊ chimeric mice on LDLR ؊/؊ background were generated. Early fatty streak lesion formation in these mice was not affected by leukocyte CXCR2 deficiency whereas lesions were less developed in mice lacking leukocyte CXCR2 when atherosclerosis was allowed to progress to the intermediate stage.

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Interleukin-8 Production by Macrophages From Atheromatous Plaques

Cited by 142 publications

References 21 publications

Prostaglandin E2 Suppresses Chemokine Production in Human Macrophages through the EP4 Receptor

Prostaglandin E2 Suppresses Chemokine Production in Human Macrophages through the EP4 Receptor

Treponema denticola induces interleukin-8 and macrophage chemoattractant protein 1 production in human umbilical vein epithelial cells

Up-Regulated Expression of the CXCR2 Ligand KC/GRO-α in Atherosclerotic Lesions Plays a Central Role in Macrophage Accumulation and Lesion Progression

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