Prevention of collagen-induced arthritis by oral administration of encapsulated Type II collagen

Thompson, H. S. G.; Harper, Nicola; Assadullahi, T; Hider, Robert C.; Staines, N. A.

doi:10.1007/978-94-009-1848-1_75

Cited by 17 publications

(27 citation statements)

References 6 publications

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“…35 However, the participation of the Th1-type response in the susceptibility to PIA was also observed in other mouse models, with arthritic animals producing higher levels of IFNg and IL-2 in comparison to resistant mice. 7 In relation to the Slc11a1 allele effect on the modulation of cytokine production, studies on Salmonella enterica serotype Typhimurium infection suggest that the resistance of Slc11a1 R mice is due to an increased production of IFNg and IL-12 by the macrophages, 19 whereas in attenuated Salmonella vaccination experiments the S allele favored IL-4 and IgE production. 36 Recently, the Slc11a1 S allele was implicated in Th2 polarization during Salmonella infection.…”

Section: Discussionmentioning

confidence: 99%

“…Pristane-induced arthritis (PIA) has proven to be a valuable experimental model for RA. In susceptible inbred mouse lines, such as BALB/c 6 and CBA Igh b , 7 15-25% of the mice developed inflammation of the ankle and wrist joints approximately 200 days after pristane injection. Susceptibility to PIA is CD4 þ T-cell (Th)-dependent 8 and has been associated with increased agalactosyl IgG levels mediated by IL-6 production.…”

Section: Introductionmentioning

confidence: 99%

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Slc11a1 (formerly NRAMP1) gene modulates both acute inflammatory reactions and pristane-induced arthritis in mice

et al. 2006

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Mice selected for the maximum acute inflammatory reaction (AIRmax) are highly susceptible to pristane-induced arthritis (PIA), whereas mice selected for the minimum response (AIRmin) are resistant. These lines show distinct patterns of leukocyte infiltration and R and S allele frequency disequilibrium of the solute carrier family 11a member 1 (Slc11a1) gene. In order to study the interactions of the Slc11a1 R and S alleles with the inflammation modulating Quantitative Trait Loci (QTL) during PIA development, homozygous AIRmax RR , AIRmax SS , AIRmin RR and AIRmin SS lines were produced by genotype-assisted breedings. These mice received two intraperitoneal injections of 0.5 ml pristane at 60-day intervals, and the subsequent development of arthritis was assessed for 210 days. Cytokine-secreting cell profiles were investigated using enzyme-linked immunospot. Arthritis incidence in AIRmax RR mice reached 29%, whereas PIA incidence in AIRmax SS mice was 70% by day 180. AIRmin RR mice were resistant, whereas 13.3% of AIRmin SS mice became arthritic. The presence of the defective S allele also increased arthritis severity, although acute inflammation was higher in mice bearing the R allele. A predominant Th0/Th2-type response in Slc11a1 SS mice was observed. These results indicate that Slc11a1 is a strong candidate for the QTL modulating acute inflammation and for PIA.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Slc11a1 (formerly NRAMP1) gene modulates both acute inflammatory reactions and pristane-induced arthritis in mice

et al. 2006

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“…O ral administration of Ag to ameliorate autoimmune disease has been demonstrated in a number of experimental animal models (1)(2)(3). Recently, trials have been initiated to assess the feasibility of such treatments in the reduction of human disease (4).…”

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confidence: 99%

“…Such regulatory cells have been shown to be capable of transferring tolerance to naive recipients. In an experimental allergic encephalomyelitis (EAE) 3 model, the cells that transferred this tolerance following oral administration of Ag were CD8 ϩ T cells (14). An important role of CD8 ϩ regulatory T cells in the generation and maintenance of oral tolerance has also been suggested by experimentation in other models (15,16).…”

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Oral Exposure to Alloantigen Generates Intragraft CD8+ Regulatory Cells

Zhou

Carr

Liwski

et al. 2001

The Journal of Immunology

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We have previously reported that oral administration of allogeneic rat spleen cells before kidney allotransplantation significantly prolongs graft survival. This prolongation was alloantigen specific and was associated with a decrease in graft-infiltrating cells (GIC) and an increase in transcription of IL-4 mRNA in the GIC. In this study increased splenic mixed lymphocyte responses from animals orally exposed to alloantigen before kidney transplantation suggested that the kidney allograft prolongation was not due to a masking of allorecognition, but to an immunomodulation of the immune response. We have assessed GIC T cell subsets on day 5 post-transplant and found decreased numbers of CD4+ T cells in fed animals compared with controls, but there was no change in CD8+ T cell numbers. The CD8+ GIC from fed animals transcribed substantial levels of perforin, granzyme, and Fas ligand mRNA, indicating the presence of active CTL. Direct CTL assays showed that the GIC from fed recipients exhibited higher allo-CTL activity than GIC from control unfed recipients. In addition, the CD8+ GIC exhibited high levels of IL-4 mRNA, suggesting Tc2-type regulatory cells. Prolonged graft survival in the face of active CTL and Tc2 cells suggests the presence of a CD8+ regulatory cell population in the allograft. To confirm this, cell transfer experiments were performed. Prolongation of graft survival was transferred from rats orally exposed to alloantigen to naive animals by transfer of CD8+ GIC. This is the first report that oral exposure to alloantigen prolongs kidney allograft survival by the generation of intragraft CD8+ regulatory cells.

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“…However, the role of immunity to CII in RA is unclear. Oral administration of CII has been shown to suppress collagen-induced (4,5), adjuvant (6), and pristane-induced arthritis (7). Furthermore, it has been possible to adoptively transfer suppression from CII-fed animals to naive animals in both the collagen-induced (4) and adjuvant arthritis models (6).…”

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confidence: 99%

Suppression of antigen‐induced arthritis in lewis rats by oral administration of type ii collagen

Yoshino

Quattrocchi

Weiner

1995

Arthritis & Rheumatism

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Objective. To assess the effect of orally administered type I1 collagen (CII) in antigen-induced arthritis (AIA).Methods. Arthritis was induced in Lewis rats by immunization with methylated bovine serum albumin (mBSA) in Freund's complete adjuvant, followed by an intraarticular injection of mBSA 2 weeks later. Different doses of CII, mBSA, and an unrelated control protein, keyhole limpet hemocyanin (KLH), were orally administered 5 times over several days prior to the induction of arthritis. Ankle joint swelling and delayed-type hypersensitivity (DTH) responses were measured.Results. Joint swelling was significantly reduced at a dose of 3 p g and 30 p g of CII, but not at 300 pg. The most prominent suppression of AIA was observed when rats were fed 10 mg of mBSA, whereas oral KLH had no effect. DTH responses were significantly reduced in the mBSA-fed rats, but not in rats that were fed CII or KLH.Conclusion. Oral CII can suppress arthritis in an animal model in which immunity to collagen does not play a role. The effect is dose dependent and occurs at lower doses of CII. These results demonstrate the biologic relevance of bystander suppression associated with oral tolerance, and the potential use of this approach to treat human inflammatory joint disease.

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Prevention of collagen-induced arthritis by oral administration of encapsulated Type II collagen

Cited by 17 publications

References 6 publications

Slc11a1 (formerly NRAMP1) gene modulates both acute inflammatory reactions and pristane-induced arthritis in mice

Slc11a1 (formerly NRAMP1) gene modulates both acute inflammatory reactions and pristane-induced arthritis in mice

Oral Exposure to Alloantigen Generates Intragraft CD8+ Regulatory Cells

Suppression of antigen‐induced arthritis in lewis rats by oral administration of type ii collagen

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