Mice transgenic for intracellular interleukin‐1 receptor antagonist type 1 are protected from collagen‐induced arthritis

Palmer, Gaby; Talabot-Ayer, Dominique; Szalay-Quinodoz, Ildiko; Maret, Michel; Arend, William P.; Gabay, Cem

doi:10.1002/immu.200310018

Cited by 29 publications

(23 citation statements)

References 24 publications

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“…For example, treatment of rheumatoid arthritis patients with chimeric mAbs to TNF-␣ significantly improved major clinical end points of the disease process, including a decrease in SAA (31). Transgenic mice overexpressing IL-1R antagonist were protected from collagen-induced arthritis, with reduced level of circulating A-SAA (32). We demonstrated that bortezomib can transiently inhibit the induction of luciferase expression at the knee joint after zymosan administration.…”

Section: Figurementioning

confidence: 79%

Serum Amyloid A-Luciferase Transgenic Mice: Response to Sepsis, Acute Arthritis, and Contact Hypersensitivity and the Effects of Proteasome Inhibition

Zhang¹,

Ahsan²,

Purchio³

et al. 2005

The Journal of Immunology

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Acute phase serum amyloid A proteins (A-SAAs) are multifunctional apolipoproteins produced in large amounts during the acute phase of an inflammation and also during the development of chronic inflammatory diseases. In this study we present a Saa1-luc transgenic mouse model in which SAA1 gene expression can be monitored by measuring luciferase activity using a noninvasive imaging system. When challenged with LPS, TNF-α, or IL-1β, in vivo imaging of Saa1-luc mice showed a 1000- to 3000-fold induction of luciferase activity in the hepatic region that peaked 4–7 h after treatment. The induction of liver luciferase expression was consistent with an increase in SAA1 mRNA in the liver and a dramatic elevation of the serum SAA1 concentration. Ex vivo analyses revealed luciferase induction in many tissues, ranging from several-fold (brain) to >5000-fold (liver) after LPS or TNF-α treatment. Pretreatment of mice with the proteasome inhibitor bortezomib significantly suppressed LPS-induced SAA1 expression. These results suggested that proteasome inhibition, perhaps through the NF-κB signaling pathway, may regulate SAA1 expression. During the development of acute arthritis triggered by intra-articular administration of zymosan, SAA1 expression was induced both locally at the knee joint and systemically in the liver, and the induction was significantly suppressed by bortezomib. Induction of SAA1 expression was also demonstrated during contact hypersensitivity induced by topical application of oxazolone. These results suggest that both local and systemic induction of A-SAA occur during inflammation and may contribute to the pathogenesis of chronic inflammatory diseases associated with amyloid deposition.

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Section: Figurementioning

confidence: 79%

Serum Amyloid A-Luciferase Transgenic Mice: Response to Sepsis, Acute Arthritis, and Contact Hypersensitivity and the Effects of Proteasome Inhibition

Zhang¹,

Ahsan²,

Purchio³

et al. 2005

The Journal of Immunology

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“…For instance, a 67-amino acid sequence of MCP-1 that specifically antagonizes MCP-1 abrogated arthritis in MRL-lpr autoimmune mice, and an antagonist of RANTES ameliorated CIA in mice (47)(48)(49). IL-1 receptor antagonist protein, a naturally produced specific antagonist of IL-1␤, has consistently shown potent antiinflammatory properties in animal models of inflammation (50)(51)(52) and is used in the treatment of RA (53)(54)(55)(56)(57)(58). CXCL16 is a novel chemokine that has not been fully characterized in chronic disease, and it is especially of interest because its only known receptor to date has been shown to be highly expressed in chronic Th1 diseases such as RA (28).…”

Section: Discussionmentioning

confidence: 99%

CXCL16‐mediated cell recruitment to rheumatoid arthritis synovial tissue and murine lymph nodes is dependent upon the MAPK pathway

Ruth¹,

Haas²,

Park³

et al. 2006

Arthritis & Rheumatism

107

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Objective. Rheumatoid arthritis (RA) is characterized by profound mononuclear cell (MNC) recruitment into synovial tissue (ST), thought to be due in part to tumor necrosis factor ␣ (TNF␣), a therapeutic target for RA. Although chemokines may also be involved, the mechanisms remain unclear. We undertook this study to examine the participation of CXCL16, a novel chemokine, in recruitment of MNCs to RA ST in vivo and to determine the signal transduction pathways mediating this process. Conclusion. Taken together, these results point to a unique role for CXCL16 as a premier MNC recruiter in RA and suggest additional therapeutic possibilities, targeting CXCL16, its receptor, or its signaling pathways.

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“…Total RNA was extracted from 1 · 10 6 BMMC, P815 cells, 3T3 murine fibroblasts, ATDC5 mouse chondrocytes or from joints of mice with collagen induced arthritis [13] with TRIzol (Invitrogen) according to the manufacturer's protocol.…”

Section: Rna Extractionmentioning

confidence: 99%

Interleukin (IL)-33 induces the release of pro-inflammatory mediators by mast cells

Donzé²,

et al. 2007

Self Cite

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IL-33 (or IL-1F11) was recently identified as a ligand for the previously orphaned IL-1 family receptor T1/ST2. Previous studies have established that IL-33 and T1/ST2 exert key functions in Th2 responses. In this study, we demonstrate that IL-33 induces the production of pro-inflammatory mediators in mast cells. IL-33 dose and time-dependently stimulated IL-6 secretion by P815 mastocytoma cells and primary mouse bone marrow-derived mast cells (BMMC). This effect was dependent on T1/ST2 binding. In addition, IL-33 also induced IL-1b, TNF-a, MCP-1, and PGD2 production in BMMC. By RNase protection assay, we demonstrated that IL-33 increased IL-6 and IL-1b mRNA expression. These effects of IL-33 appeared to occur independently of mast cell degranulation, The results of this study show for the first time that IL-33, a novel member of the IL-1 family of cytokines, stimulates the production of pro-inflammatory mediators by mast cells in addition to its effect on T helper 2 responses. These findings open new perspectives for the treatment of inflammatory diseases by targeting IL-33.

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Mice transgenic for intracellular interleukin‐1 receptor antagonist type 1 are protected from collagen‐induced arthritis

Cited by 29 publications

References 24 publications

Serum Amyloid A-Luciferase Transgenic Mice: Response to Sepsis, Acute Arthritis, and Contact Hypersensitivity and the Effects of Proteasome Inhibition

Serum Amyloid A-Luciferase Transgenic Mice: Response to Sepsis, Acute Arthritis, and Contact Hypersensitivity and the Effects of Proteasome Inhibition

CXCL16‐mediated cell recruitment to rheumatoid arthritis synovial tissue and murine lymph nodes is dependent upon the MAPK pathway

Interleukin (IL)-33 induces the release of pro-inflammatory mediators by mast cells

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