scholarly journals Bosentan may induce arthritis flare in patients with scleroderma concomitantly treated with methotrexate

2006 ◽  
Vol 65 (5) ◽  
pp. 692-693 ◽  
Author(s):  
F Cozzi
Keyword(s):  
1991 ◽  
Vol 4 (6) ◽  
pp. 871-880 ◽  
Author(s):  
Sandra Kleinau ◽  
Helena Erlandsson ◽  
Rikard Holmdahl ◽  
Lars Klareskog
Keyword(s):  

1990 ◽  
Vol 171 (1) ◽  
pp. 339-344 ◽  
Author(s):  
M E Billingham ◽  
S Carney ◽  
R Butler ◽  
M J Colston

A recombinant (r)65-kD protein from Mycobacterium leprae, at levels far in excess of those present in whole mycobacteria, was unable to induce arthritis. Even when combined with a synthetic adjuvant, CP20961, to mimic the peptidoglycan adjuvant component of the mycobacterial cell wall, the r65-kD protein failed to induce arthritis. Pretreatment with as little as 1 microgram r65-kD protein protected rats against arthritis induced by M. tuberculosis, but this r65-kD protein was markedly less able to protect against arthritis induced by the synthetic adjuvant, CP20961, or type II collagen. The r65-kD protein appears, therefore, to produce an antigen-specific protection against arthritis induced by bacterial cell walls containing the 65-kD protein. Such protection can be overcome, however, by arthritogenic T lymphocytes, suggesting that protection occurs by preventing clonal proliferation of autoreactive T lymphocytes that are induced by the adjuvant properties of mycobacterial cell walls. How the r65-kD protein abrogates this particular adjuvant activity, and the nature of the arthritogenic self antigen(s), remain to be elucidated.


1997 ◽  
Vol 115 (2) ◽  
pp. 1406-1409 ◽  
Author(s):  
Waldenise Cossermelli-Messina ◽  
Wilson Cossermelli

Microbial agents induce arthritis through mechanisms such as direct infiltration of tissue and by inducing autoimmune phenomena. The mechanisms involved in this last type of arthritis have been investigated. In experimental models of adjuvant and reactive arthritis, the involvement of T cells and in some cases mycobacteria in the development of arthritis have been confirmed. Cross-reactivity between the 65 kD mycobacterial protein and cartilage proteoglycans has been postulated as a possible mechanism. In this study, chronic peripheral arthritis was observed in patients with Hansen's disease, in patients with resolved Hansen's and in those with paucibacillary forms. This arthritis was not related to reactional states (erythema nodosum Ieprosum and reversal reaction), in contrast to several reports in the literature. The mechanisms by which microbes could induce chronic arthritis are discussed herein.


2021 ◽  
Vol 12 ◽  
Author(s):  
Yunjuan Zhao ◽  
Vilma Urbonaviciute ◽  
Bingze Xu ◽  
Weiwei Cai ◽  
Zeynep Sener ◽  
...  

The most commonly used strains in experimental research, including genetically modified strains, are C57BL/6 mice. However, so far, no reliable model for rheumatoid arthritis is available, mainly due to the restriction by the MHC class II haplotype H-2b. Collagen-induced arthritis (CIA) is the most widely used animal model of rheumatoid arthritis, but C57BL/6 strain is resistant to CIA because there is no collagen II peptide associated with H-2b. To establish a rheumatoid arthritis model in C57BL/6 mice, we immunized C57BL/6NJ (B6N) mice with human cartilage oligomeric matrix protein (COMP), which induced severe arthritis with high incidence, accompanied by a strong auto-antibody response. Native COMP was required, as denatured COMP lost its ability to induce arthritis in B6N mice. An immunodominant COMP peptide was identified as the key T cell epitope, with a perfect fit into the Ab class II peptide binding pocket. A critical amino acid in this peptide was found to be phenylalanine at position 95. Recombinant COMP mutated at position 95 (COMP_F95S) lost its ability to induce arthritis or a strong immune response in the B6N mice. In conclusion, A new model for RA has been established using C57BL/6 mice through immunization with COMP, which is dependent on a COMP specific peptide binding Ab, thus in similarity with CIA in Aq expressing strains.


2019 ◽  
Vol 56 (2) ◽  
pp. 113-117
Author(s):  
Jacqueline Nelisis ZANONI ◽  
Gleison Daion PIOVEZANA BOSSOLANI

ABSTRACT BACKGROUND: Few studies regarding arthritic diseases have been performed to verify the presence of the neurodegeneration. Given the increased oxidative stress and extra-articular effects of the rheumatoid arthritis, the gastrointestinal studies should be further investigated aiming a better understanding of the systemic effects the disease on enteric nervous system. OBJECTIVE: To determine whether the rheumatoid arthritis affects the nitrergic density and somatic area of the nNOS- immunoreactive (IR) myenteric neurons, as well as the morphometric areas of CGRP and VIP-IR varicosities of the ileum of arthritic rats. METHODS: Twenty 58-day-old male Holtzmann rats were distributed in two groups: control and arthritic. The arthritic group received a single injection of the Freund’s Complete Adjuvant in order to induce arthritis model. The whole-mount preparations of ileum were processed for immunohistochemistry to VIP, CGRP and nNOS. Quantification was used for the nitrergic neurons and morphometric analyses were performed for the three markers. RESULTS: The arthritic disease induced a reduction 6% in ileal area compared to control group. No significant differences were observed in nitrergic density comparing both groups. However, arthritic group yielded a reduction of the nitrergic neuronal somatic area and VIP-IR varicosity areas. However, an increase of varicosity CGRP-IR areas was also observed. CONCLUSION: Despite arthritis resulted in no alterations in the number of nitrergic neurons, the retraction of ileal area and reduction of nitrergic somatic and VIP-IR varicosity areas may suggest a negative impact the disease on the ENS.


1988 ◽  
Vol 17 (2) ◽  
pp. 131-141 ◽  
Author(s):  
K. J. Pulkki ◽  
E. T. Eerola ◽  
R. M. Saario ◽  
A. Toivanen ◽  
E. I. Vuorio

2011 ◽  
Vol 179 (5) ◽  
pp. 2490-2500 ◽  
Author(s):  
Akhilesh Kumar Shakya ◽  
Ashok Kumar ◽  
Dorota Klaczkowska ◽  
Malin Hultqvist ◽  
Kristin Hagenow ◽  
...  

2013 ◽  
Vol 95 (4) ◽  
pp. 661-666 ◽  
Author(s):  
S. C. Narendra ◽  
J. P. Chalise ◽  
N. Hook ◽  
M. Magnusson

2019 ◽  
Vol 20 (4) ◽  
pp. S28
Author(s):  
L. Qu ◽  
L. Wang ◽  
X. Jiang ◽  
Q. Zheng ◽  
S. Jeon ◽  
...  

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