Local expression of the serum amyloid A and formyl peptide receptor–like 1 genes in synovial tissue is associated with matrix metalloproteinase production in patients with inflammatory arthritis

O'Hara, Rosemary; Murphy, Evelyn P.; Whitehead, Alexander S.; FitzGerald, Oliver; Bresnihan, Barry

doi:10.1002/art.20301

Cited by 131 publications

(135 citation statements)

References 41 publications

Supporting

Mentioning

118

Contrasting

Unclassified

Order By: Relevance

“…The first one entails the pivotal role played by TNFα, but not other cytokines tested, in activating the Fpr2/3 gene promoter, as demonstrated using a combination of reporter assays ex vivo and in vitro, with analyses in mouse and human cells. The appreciation that proinflammatory mediators set in motion the resolution and protective phase of inflammation is emerging (42), yet our data solidly show this link and identify TNFα as the culprit, acting through the type I receptor. This set of data extends previous in vitro observations in synovial fibroblasts (43) and mouse microglial cells (44).…”

Section: Discussionmentioning

confidence: 64%

Nonredundant protective properties of FPR2/ALX in polymicrobial murine sepsis

Gobbetti

Coldewey

Chen

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

105

104

View full text Add to dashboard Cite

Significance Sepsis defines a syndrome with poor clinical management characterized by overlapping phases of excessive inflammation temporally aligned with an immunosuppressed state. We define an endogenous pathway centered on formyl-peptide receptor 2/3 (Fpr2/3)—ortholog to human FPR2/ALX (receptor for lipoxin A4)—that protects the host against polymicrobial sepsis. Using null mice and proof-of-concept experiments with a peptide–agonist, we demonstrate how engagement of Fpr2/3 is crucial to enact nonredundant functions that span from control of cell recruitment and phagocytosis, modulation of soluble mediator generation, to containment of bacteremia, thus preventing spreading to vital organs and opening new opportunities to manipulate the host response in sepsis.

show abstract

Section: Discussionmentioning

confidence: 64%

Nonredundant protective properties of FPR2/ALX in polymicrobial murine sepsis

Gobbetti

Coldewey

Chen

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

105

104

View full text Add to dashboard Cite

show abstract

“…SAA, unlike CRP, can also directly activate monocyte TF expression. Thus, in inflammatory lesions, the local production of SAA by activated macrophages (43,44) could generate a positive feedback loop even in the absence of lymphocytes.…”

Section: Discussionmentioning

confidence: 99%

“…Soluble RAGE [42][43][44][45][46][47][48][49][50][51][52][53][54][55][56][57][58][59] (sRAGE) and the reverse peptide were synthesized by manual solid-phase synthesis using 2-(1H-benzotriazole-1-yl)-1,1,3,3-tetramethyluronium hexafluorophosphate-mediated couplings with Boc in situ neutralization chemistry (27) and purified by preparative reverse-phase HPLC using a C 18 column. Fractions containing the pure proteins were rerun on analytical HPLC, and masses were confirmed by electrospray ionization mass spectrometry (21,765.5 Ϯ 1.0, calculated: 2,177.2).…”

Section: Reagentsmentioning

confidence: 99%

See 1 more Smart Citation

Serum Amyloid A Induces Monocyte Tissue Factor

Cai

Song

Endoh

et al. 2007

The Journal of Immunology

106

121

View full text Add to dashboard Cite

C-reactive protein (CRP) and serum amyloid A (SAA) increase in the blood of patients with inflammatory conditions and CRP-induced monocyte tissue factor (TF) may contribute to inflammation-associated thrombosis. This study demonstrates that SAA is a potent and rapid inducer of human monocyte TF. SAA induced TF mRNA in PBMC within 30 min and optimal procoagulant activity within 4 h, whereas CRP (25 μg/ml)-induced activity was minimal at this time. Unlike CRP, SAA did not synergize with LPS. Procoagulant activity was inhibited by anti-TF and was dependent on factors VII and X, and TF Ag levels were elevated on CD14+ monocytes. Responses were optimal with lymphocytes, although these were not obligatory. Inhibitor studies indicate activation of NF-κB through the ERK1/2 and p38 MAPK pathways; the cyclo-oxygenase pathway was not involved. SAA-induced TF was partially inhibited by high-density lipoprotein, but not by low-density lipoprotein or by apolipoprotein A-I. SAA is a ligand for the receptor for advanced glycation end products (RAGE), and TF generation was suppressed by ∼50% by a RAGE competitor, soluble RAGE, and by ∼85% by anti-RAGE IgG. However, another RAGE ligand, high mobility group box-1 protein, capable of inducing monocyte chemotactic protein-1 mRNA in 2 h, did not induce TF within 24 h. Cross-linking studies confirmed SAA binding to soluble RAGE. Elevated SAA is a marker of disease activity in patients with rheumatoid arthritis, and PBMC from patients with rheumatoid arthritis were more sensitive to SAA than normals, suggesting a new link between inflammation and thrombosis.

show abstract

“…Finally, another study suggested that serum amyloid A is highly expressed by the inflamed human synovial tissue and could bind to formyl peptide receptor-like 1 amplifying the inflammatory response in the synovium [64]. It was also demonstrated that besides proinflammatory cytokines, serum amyloid A, could independently stimulate the release of MMP-1 and MMP-3 from endothelial and fibroblast-like synoviocytes isolated from patients with PsA [64].…”

Section: Bone Remodeling and Metalloproteinasesmentioning

confidence: 99%

Immunopathogenesis of psoriatic arthritis: Recent advances

et al. 2008

View full text Add to dashboard Cite

AbstractPsoriatic Arthritis (PsA) is a chronic inflammatory arthritis associated with psoriasis. The pathophysiology of PsA includes genetic, environmental and immunologic factors. Recent studies revealed the dynamic role of the immune system in the pathogenesis of the disease. Adhesion molecules, proinflammatory cytokines, angiogenic factors and metalloproteinases appear to orchestrate the inflammatory response in PsA. This article summarizes the current immunologic findings and suggests future therapeutic and researching approaches in the field of PsA.

show abstract

Local expression of the serum amyloid A and formyl peptide receptor–like 1 genes in synovial tissue is associated with matrix metalloproteinase production in patients with inflammatory arthritis

Cited by 131 publications

References 41 publications

Nonredundant protective properties of FPR2/ALX in polymicrobial murine sepsis

Nonredundant protective properties of FPR2/ALX in polymicrobial murine sepsis

Serum Amyloid A Induces Monocyte Tissue Factor

Immunopathogenesis of psoriatic arthritis: Recent advances

Contact Info

Product

Resources

About