The Effects of Recombinant Human Granulocyte Colony-Stimulating Factor on Passive Collagen-Induced Arthritis Transferred with Anti-Type II Collagen Antibody

Miyahara, Hisaaki; Hotokebuchi, Takao; Saikawa, Isao; Arita, Chikafumi; Takagishi, Kenji; Sugioka, Yôichi

doi:10.1006/clin.1993.1151

Cited by 14 publications

(9 citation statements)

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“…Neutrophils and their migration into the joint have been implicated in the onset of clinical arthritis and in the regulation of disease activity and severity (5)(6)(7)(8)(9)(10)(11)(12)(13). Therefore, understanding the regulation of neutrophil migration into the synovial tissue and fluid, and neutrophil functional regulation could be a critical step toward generating more effective therapies for arthritis.…”

Section: Discussionmentioning

confidence: 99%

“…Neutrophils are also present in increased numbers in RA synovial fluid, and are the predominant cell type present during flare-up (10). Additionally, neutrophils are required for the development of experimental arthritis (6,11,12), and neutropenia in RA, as seen in Felty's syndrome, is associated with reduced joint inflammation (13). Taken together, current evidence implicates neutrophils and their migration into the joint as central to the onset of arthritis and to the regulation of disease activity and severity.…”

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confidence: 98%

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The Arthritis Severity Quantitative Trait Loci Cia4 and Cia6 Regulate Neutrophil Migration into Inflammatory Sites and Levels of TNF-α and Nitric Oxide

Laragione

Yarlett

Mello

et al. 2007

The Journal of Immunology

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Neutrophils are required for the development of arthritis, and their migration into the synovial tissue coincides with the onset of clinical disease. Synovial neutrophil numbers also correlate with rheumatoid arthritis disease activity and severity. We hypothesized that certain arthritis severity genes regulate disease via the regulation of neutrophil migration into the joint. This hypothesis was tested in the synovial-like air pouch model injected with carrageenan using arthritis-susceptible DA and arthritis-resistant F344 rats. DA had nearly 3-fold higher numbers of exudate neutrophils compared with F344 (p < 0.001). Five DA.F344(QTL) strains congenic for severity loci and protected from autoimmune arthritis were studied. Only DA.F344(Cia4) (chromosome 7) and DA.F344(Cia6) (chromosome 8) congenics had significantly lower exudate neutrophil counts compared with DA. TNF-α levels were 2.5-fold higher in DA exudates as compared with F344 exudates, and that difference was accounted for by the Cia4 locus. Exudate levels of NO, a known inhibitor of neutrophil chemotaxis, were higher in F344, compared with DA, and that difference was accounted for by Cia6. This is the first time that non-MHC autoimmune arthritis loci are found to regulate three central components of the innate immune response implicated in disease pathogenesis, namely neutrophil migration into an inflammatory site, as well as exudate levels of TNF-α and NO. These observations underscore the importance of identifying the Cia4 and Cia6 genes, and suggest that they should generate useful novel targets for development of new therapies.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 98%

The Arthritis Severity Quantitative Trait Loci Cia4 and Cia6 Regulate Neutrophil Migration into Inflammatory Sites and Levels of TNF-α and Nitric Oxide

Laragione

Yarlett

Mello

et al. 2007

The Journal of Immunology

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“…Contradictory results have been obtained with the administration of exogenous G-CSF being reported to prevent adjuvant-arthritis in rats (75) but to exacerbate murine collagen-induced arthritis (76) and a passive transfer model of collagen-induced arthritis in rats (77). The deleterious role of G-CSF (Fig.…”

Section: G-csf In Preclinical Models Of Autoimmune Diseasesmentioning

confidence: 96%

Granulocyte Colony-Stimulating Factor: A Novel Mediator of T Cell Tolerance

Rutella

Zavala

Danese

et al. 2005

The Journal of Immunology

201

154

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In recent years, several investigators have unraveled a previously unrecognized role for G-CSF in the regulation of T cell and dendritic cell functions. The experimental evidence in favor of G-CSF-mediated immune regulation includes the ability to switch T cell cytokine secretion profile to Th2 responses and the promotion of regulatory T cell and tolerogenic dendritic cell differentiation. Interestingly, G-CSF is beneficial in animals for the prevention and/or treatment of immune-mediated diseases, e.g., graft-vs-host disease, multiple sclerosis, systemic lupus erythematosus, inflammatory bowel disease, and diabetes, suggesting a potential role in human autoimmune diseases. This review summarizes the growing body of evidence that supports a critical role for G-CSF as a novel mediator of T cell tolerance.

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“…Both granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) have been shown to flare arthritis in mice. 14,15 Anecdotal clinical reports have reported exacerbation of autoimmune disease following treatment with G-CSF and GM-CSF. These have largely been in the context of Felty's syndrome [16][17][18][19][20][21] or drug-induced neutropenia.…”

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confidence: 99%

A randomised, blinded, placebo-controlled, dose escalation study of the tolerability and efficacy of filgrastim for haemopoietic stem cell mobilisation in patients with severe active rheumatoid arthritis

Snowden

Biggs

Milliken

et al. 1998

Bone Marrow Transplant

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Summary:Autologous haemopoietic stem cell transplantation (HSCT) represents a potential therapy for severe rheumatoid arthritis (RA). As a prelude to clinical trails, the safety and efficacy of haemopoietic stem cell (HSC) mobilisation required investigation as colony-stimulating factors (CSFs) have been reported to flare RA. A double-blind, randomised placebo-controlled dose escalation study was performed. Two cohorts of eight patients fulfilling strict eligibility criteria for severe active RA (age median 40 years, range 24-60 years; median disease duration 10.5 years, range 2-18 years) received filgrastim (r-Hu-methionyl granulocyte(G)-CSF) at 5 and 10 g/kg/day, randomised in a 5:3 ratio with placebo. Patients were unblinded on the fifth day of treatment and those randomised to filgrastim underwent cell harvesting (leukapheresis) daily until 2 ؋ 10 6 /kg CD34 ؉ cells (haemopoietic stem and progenitor cells) were obtained. Patients were assessed by clinical and laboratory parameters before, during and after filgrastim administration. RA flare was defined as an increase of 30% or more in two of the following parameters: tender joint count, swollen joint count or pain score. Efficacy was assessed by quantitation of CD34 ؉ cells and CFU-GM. One patient in the 5 g/kg/day group and two patients in the 10 g/kg/day group fulfilled criteria for RA flare, although this did not preclude successful stem cell collection. Median changes in swollen and tender joint counts were not supportive of filgrastim consistently causing exacerbation of disease, but administration of filgrastim at 10 g/kg/day was associated with rises in median C-reactive protein and median rheumatoid factor compared with placebo. Other adverse events were well recognised for filgrastim and included bone pain (80%) and increases in alkaline phosphatase (four-fold) and lactate dehydrogenase (two-fold). With respect to efficacy, filgrastim at 10 g/kg/day was more efficient with all patients (n = 5) achieving target CD34 ؉ cell counts with a single leuCorrespondence: Dr JA Snowden, Department of Haematology, Royal Hallamshire Hospital, Sheffield S10 2JF, UK Received 2 May 1998; accepted 21 July 1998 kapheresis (median = 2.8, range = 2.3-4.8 ؋ 10 6 /kg, median CFU-GM = 22.1, range = 4.2-102.9 ؋ 10 4 /kg), whereas 1-3 leukaphereses were necessary to achieve the target yield using 5 g/kg/day. We conclude that filgrastim may be administered to patients with severe active RA for effective stem cell mobilisation. Flare of RA occurs in a minority of patients and is more likely with 10 than 5 g/kg/day. However, on balance, 10 g/kg/day remains the dose of choice in view of more efficient CD34 ؉ cell mobilisation.

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The Effects of Recombinant Human Granulocyte Colony-Stimulating Factor on Passive Collagen-Induced Arthritis Transferred with Anti-Type II Collagen Antibody

Cited by 14 publications

References 0 publications

The Arthritis Severity Quantitative Trait Loci Cia4 and Cia6 Regulate Neutrophil Migration into Inflammatory Sites and Levels of TNF-α and Nitric Oxide

The Arthritis Severity Quantitative Trait Loci Cia4 and Cia6 Regulate Neutrophil Migration into Inflammatory Sites and Levels of TNF-α and Nitric Oxide

Granulocyte Colony-Stimulating Factor: A Novel Mediator of T Cell Tolerance

A randomised, blinded, placebo-controlled, dose escalation study of the tolerability and efficacy of filgrastim for haemopoietic stem cell mobilisation in patients with severe active rheumatoid arthritis

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