scholarly journals Persistent Analgesic Effect of Sustained Release Diclofenac Sodium Preparation on Bovine Type II Collagen-Induced Arthritis

2002 ◽  
Vol 48 (1) ◽  
pp. 48-54 ◽  
Author(s):  
Masami Takahashi ◽  
Norimitsu Umehara ◽  
Masakatsu Tezuka
Keyword(s):  
Sustained Release ◽  
Analgesic Effect ◽  
Diclofenac Sodium ◽  
Type Ii Collagen ◽  
Type Ii ◽  
Collagen Induced Arthritis ◽  
Bovine Type

scholarly journals Vaccination with an immunodominant peptide of bovine type II collagen induces an anti‐TCR response, and modulates the onset and severity of collagen‐induced arthritis

2004 ◽  
Vol 16 (5) ◽  
pp. 737-745 ◽  
Author(s):  
Aki Honda ◽  
Akio Ametani ◽  
Takashi Matsumoto ◽  
Amane Iwaya ◽  
Hiroshi Kano ◽  
...  
Keyword(s):  
Type Ii Collagen ◽  
Type Ii ◽  
Collagen Induced Arthritis ◽  
Bovine Type

Citrullinated fibrinogen is a target of auto-antibodies in interstitial lung disease in mice with collagen-induced arthritis

2020 ◽  
Vol 32 (8) ◽  
pp. 533-545
Author(s):  
Tomomi Sato ◽  
Hiroki Satooka ◽  
Satoko Ichioka ◽  
Yoshihiro Maruo ◽  
Takako Hirata
Keyword(s):  
Interstitial Lung Disease ◽  
Lung Disease ◽  
Usual Interstitial Pneumonia ◽  
Inflammatory Cells ◽  
Type Ii Collagen ◽  
Type Ii ◽  
Collagen Induced Arthritis ◽  
Citrullinated Proteins ◽  
Bovine Type ◽  
M2 Phenotype

Abstract Interstitial lung disease (ILD) is a very common and lethal complication of rheumatoid arthritis (RA), yet its pathogenesis is not well understood, in part due to the lack of adequate animal models. Although collagen-induced arthritis (CIA) is the most widely used animal model for RA, the lung involvement occurring in this model has scarcely been studied. To evaluate the suitability of CIA as a model for RA-associated ILD (RA-ILD), we immunized DBA/1 mice with bovine type II collagen and characterized lung disease in this model. Histologic analyses revealed patchy interstitial infiltration of inflammatory cells in the peripheral regions of the lung, notably in the subpleural region, in mice with CIA. This pattern resembled usual interstitial pneumonia in humans, which is the most prevalent pattern in RA-ILD. Among infiltrates in the lung, CD11bhi macrophages of the M2 phenotype were most prominently increased. IgG and C3 were deposited in the subpleural region where inflammatory cells infiltrated. The sera from CIA mice contained auto-antibodies against citrullinated proteins, which are specific and predictive markers for RA. Protein citrullination was enhanced in the lung of CIA mice compared with naive mice, and citrullinated fibrinogen was primarily targeted by these auto-antibodies. The elevation of auto-antibodies against citrullinated proteins and their deposition in the lung with patchy subpleural preponderance suggest that CIA can serve as a model to study the pathogenesis of RA-ILD.

scholarly journals Type II collagen-induced arthritis in rats. Passive transfer with serum and evidence that IgG anticollagen antibodies can cause arthritis.

1982 ◽  
Vol 155 (1) ◽  
pp. 1-16 ◽  
Author(s):  
J M Stuart ◽  
M A Cremer ◽  
A S Townes ◽  
A H Kang
Keyword(s):  
Type Ii Collagen ◽  
Passive Transfer ◽  
Type Ii ◽  
Autoimmune Process ◽  
Collagen Induced Arthritis ◽  
Collagen Antibodies ◽  
Circulating Immune Complex ◽  
Early Lesion ◽  
Anticollagen Antibodies ◽  
Bovine Type

We have found that serum from rats with type II collagen-induced arthritis, when fractionated with 50% ammonium sulfate and concentrated, would transfer arthritis to nonimmunized recipients. The arthritis in recipients developed within 18-72 h and displayed all of the major histopathologic characteristics of the early lesion in immunized animals but was transient and less severe. Although consideration was given to the possibility that a circulating immune complex was involved, no evidence of such a complex was detected. Further fractionation of the serum yielded an IgG anticollagen antibody that was fully active in transferring disease. The antibody's reaction was inhibited by the native bovine type II collagen used for immunization of donors and the antibody strongly cross-reacted with homologous type II collage but not with denatured collagen. These studies demonstrate that arthritis in rats can be induced with anti-type II collagen antibodies and suggest that an autoimmune process is involved. Because antibodies to collagen have also been detected in human rheumatic diseases, further investigation of the characteristics of collagen antibodies capable of inducing arthritis seems warranted.

The analgesic effect and possible mechanisms by which koumine alters type II collagen-induced arthritis in rats

2018 ◽  
Vol 73 (1) ◽  
pp. 217-225 ◽  
Author(s):  
Gui-Lin Jin ◽  
Jian Yang ◽  
Wan-Qing Chen ◽  
Jie Wang ◽  
Hong-Qiang Qiu ◽  
...  
Keyword(s):  
Analgesic Effect ◽  
Type Ii Collagen ◽  
Type Ii ◽  
Collagen Induced Arthritis

Acellular Fish Skin Grafts and Pig Urinary Bladder Matrix Assessed in the Collagen-Induced Arthritis Mouse Model

2018 ◽  
Vol 17 (4) ◽  
pp. 275-281 ◽  
Author(s):  
Skuli Magnusson ◽  
Hilmar Kjartansson ◽  
Baldur Tumi Baldursson ◽  
Katrin Astradsdottir ◽  
Magnus S. Ågren ◽  
...  
Keyword(s):  
Type I Collagen ◽  
Type Ii Collagen ◽  
Serum Levels ◽  
Type I ◽  
Type Ii ◽  
Collagen Induced Arthritis ◽  
Urinary Bladder Matrix ◽  
Freund’S Adjuvant ◽  
Freund's Adjuvant ◽  
Bovine Type

It is vital that cellular- and tissue-based products (CTPs) used for wound treatment do not provoke autoimmunity. In this study, the immunogenic response to extracts of 2 CTPs of piscine and porcine origin was assessed in the collagen-induced arthritis model. Male DBA/1J mice were divided into 4 groups, each composed of 7 to 9 animals. Each animal was injected with one of following to assess their immune responses: (1) bovine type II collagen (100 µg) in Freund’s adjuvant, (2) extract of piscine skin (100 µg) in Freund’s adjuvant, (3) extract of porcine urinary bladder matrix (100 µg) in Freund’s adjuvant, or (4) Freund’s adjuvant alone (control) at the beginning of the experiment and 3 weeks later. Clinical signs of arthritis were assessed from week 5 onwards, and anti-type II and anti-type I collagen antibody immunoglobulin G (IgG) serum levels were measured before injections and 8 weeks after exposure using enzyme-linked immunosorbent assays. Only the mice exposed to bovine type II collagen developed clinical arthritis accompanied by very high anti-type II collagen IgG serum levels. Anti-type II collagen IgG serum levels were also detected in the porcine group but were undetectable in the piscine skin and control groups after 8 weeks. There were no significant differences in anti-type I collagen IgG serum levels among the groups. The results showed that piscine skin did not provoke systemic autoimmunity against type II collagens in DBA/1J mice.

Effect of a novel anti-rheumatic drug, TA-383, on type II collagen-induced arthritis

1995 ◽  
Vol 17 (7) ◽  
pp. 597-603 ◽  
Author(s):  
Makoto Ueno ◽  
Kazunori Imaizumi ◽  
Takahisa Sugita ◽  
Isao Takata ◽  
Masakazu Takeshita
Keyword(s):  
Type Ii Collagen ◽  
Type Ii ◽  
Collagen Induced Arthritis ◽  
Rheumatic Drug

Evaluation of inflammatory change and bone erosion using a murine type II collagen-induced arthritis model

2010 ◽  
Vol 31 (5) ◽  
pp. 595-603 ◽  
Author(s):  
Samjin Choi ◽  
Yeon-Ah Lee ◽  
Seung-Jae Hong ◽  
Gi-Ja Lee ◽  
Sung Wook Kang ◽  
...  
Keyword(s):  
Bone Erosion ◽  
Type Ii Collagen ◽  
Inflammatory Change ◽  
Type Ii ◽  
Collagen Induced Arthritis ◽  
Arthritis Model

scholarly journals Dexamethasone Preconditioning Improves the Response of Collagen-Induced Arthritis to Treatment with Short-Term Lipopolysaccharide-Stimulated Collagen-Loaded Dendritic Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Corina Peña ◽  
David Gárate ◽  
Juan Contreras-Levicoy ◽  
Octavio Aravena ◽  
Diego Catalán ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Cd4 T Cells ◽  
Combined Treatment ◽  
Type Ii Collagen ◽  
Cytokine Profile ◽  
Clinical Disease ◽  
Type Ii ◽  
Collagen Induced Arthritis ◽  
Short Term

Background. Pharmacologically modulated dendritic cells (DCs) have been shown to restore tolerance in type II collagen-(CII-) induced arthritis (CIA). We examined the effect of dexamethasone (DXM) administration as a preconditioning agent, followed by an injection of lipopolysaccharide-(LPS-) stimulated and CII-loaded DCs on the CIA course.Methods. After CIA induction, mice pretreated with DXM were injected with 4-hour LPS-stimulated DCs loaded with CII (DXM/4hLPS/CII/DCs).Results. Mice injected with DXM/4hLPS/CII/DCs displayed significantly less severe clinical disease compared to animals receiving 4hLPS/CII/DCs alone or those in which only DXM was administered. Cytokine profile evaluation showed that CD4+ T cells from DXM/4hLPS/CII/DCs and 4hLPS/CII/DCs groups release higher IL-10 levels than those from mice receiving DXM alone or CIA mice. CD4+ T cells from all DC-treated groups showed less IL-17 release when compared to the CIA group. On the contrary, CD4+ T cells from DXM/4hLPS/CII/DCs and 4hLPS/CII/DCs groups released higher IFN-γlevels than those from CIA group.Conclusion. A combined treatment, including DXM preconditioning followed by an inoculation of short-term LPS-stimulated CII-loaded DCs, provides an improved strategy for attenuating CIA severity. Our results suggest that this benefit is driven by a modulation in the cytokine profile secreted by CD4+ T cells.

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