[31] Adjuvant arthritis

Taurog, Joel D.; Argentieri, Dennis; McReynolds, Richard A.

doi:10.1016/0076-6879(88)62089-1

Cited by 106 publications

(88 citation statements)

References 28 publications

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“…Adjuvant arthritis was elicited in male Lewis rats (175-200 g) by injection of 0.1 ml of Mycobacterium butyricum (Difco, Detroit, MI, USA; 10 mg/ml) in mineral oil into the base of the tail. 26 Paw volumes were measured at the beginning of the experiment by using a water displacement plethysmometer. Animals were housed in propylene cages with food and water ad libitum.…”

Section: Adjuvant Arthritismentioning

confidence: 99%

Potential role of heme oxygenase-1 in the progression of rat adjuvant arthritis

Devesa

Ferrándiz

Guillén

et al. 2005

Laboratory Investigation

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Rat adjuvant arthritis is an experimental model widely used to evaluate etiopathogenetic mechanisms in chronic inflammation. We have examined the participation of heme oxygenase-1 (HO-1) in this experimental arthritis. In this study, an increased nitric oxide (NO) production in the paw preceded the upregulation of HO-1, whereas selective inhibition of inducible NO synthase (iNOS) after the onset of arthritis decreased HO-1 expression, suggesting that the induction of this enzyme may depend on NO produced by iNOS. Therapeutic administration of the HO-1 inhibitor tin protoporphyrin IX was able to control the symptoms of arthritis. This agent significantly decreased leukocyte infiltration, hyperplastic synovitis, erosion of articular cartilage and osteolysis, as well as the production of inflammatory mediators. In this experimental model, HO-1 can be involved in vascular endothelial growth factor production and angiogenesis. These results support a role for HO-1 in mediating the progression of the disease in this model of chronic arthritis.

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Section: Adjuvant Arthritismentioning

confidence: 99%

Potential role of heme oxygenase-1 in the progression of rat adjuvant arthritis

Devesa

Ferrándiz

Guillén

et al. 2005

Laboratory Investigation

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“…Arthritis was induced by plantar injection of complete Freund's type adjuvant (CFA) in one hind footpad [17]. Animals were treated with a dosis of 100 ~tl of CFA (Mycobacterium sp.…”

Section: Animals and Tissue Preparationmentioning

confidence: 99%

Up‐regulation of cyclooxygenase‐2 mRNA in the rat spinal cord following peripheral inflammation

et al. 1996

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Prostaglandins (PG) have been described as mediators in spinal nociceptive processing after peripheral inflammation. Enzymes essential for PG biosynthesis, cyclooxygenase isozymes COX-1 and COX-2, have not yet been investigated in the spinal cord. In two studies on rats with adjuvant-induced peripheral inflammation levels of mRNA expression of both COX isoforms were analyzed in the lumbar section of the spinal curd using reverse transcription-polymerase chain reaction (RT-PCR) technique. We could show that mRNA of both COX isoforms is expressed constitutively in the spinal cord with COX-2 as the predominant isoform. Six hours after induction of peripheral inflammation, levels of COX-2 mRNA expression were raised significantly in respect to untreated control rats and returned to baseline within 3 days after induction of inflammation. COX-2 might therefore be regarded as the COX isozyme responsible for spinal PG release in nociceptive processing under a peripheral inflammatory stimulus.l~ey words: Cyclooxygenase-2; Inflammation; Spinal cord; R F-PCR densa of the kidney [8] the testis or the brain, where COX-2 is not only expressed constitutively but also considered to be the dominating COX isoform [9][10][11]. In the central nervous system (CNS) prostaglandins maintain important functions as neuroregulators [12]. It has been reported that PGs are released from the spinal cord by various processes as stimulation of afferent nerves [13], noxious thermal stimulation [14] and by increased potassium levels [15]. Prostaglandins are also known to be involved in transmission of nociceptive information in the spinal cord after peripheral inflammation [16]. Functional evidence thus indicates a role for cyclooxygenases in the spinal cord, expression of the enzyme itself, however, has not yet been investigated. We conducted two studies to determine the spinal presence and distribution of COX isozymes using the rat model of adjuvant-induced inflammation. Tissue samples of hindpaws and the lumbar section of the spinal cord were taken before and after induction of inflammation and examined for levels of COX mRNA expression by reverse transcription-polymerase chain reaction (RT-PCR).

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“…Each paw was given a score between 0 and 4, the highest score being 16 per rat. Arthritis was also confirmed and evaluated by examination of radiographs (Taurog et al, 1988;Yang et al, 1990). Rats were anaesthetized with Evipan-sodium (100 mg/kg, Bayer) and radiographs were taken for fore and hind limbs of rats with a Mammomat (Siemens), on Kodak Xomat MA film exposed at 30 kV for 160 msec.…”

Section: Induction and Evaluation Of Arthritismentioning

confidence: 99%

“…The day of arthritis induction was designated as day 0. Rats were examined daily for clinical signs of arthritis (erythema, swelling and deformity) and an arthritis index assigned as described (Taurog et al, 1988): 0, no evidence of disease; 1, inflammation of small digital joints; 2, inflammation of ankle and joints; 3 inflammation of foot-pad; and 4, inflammation of entire foot. Each paw was given a score between 0 and 4, the highest score being 16 per rat.…”

Section: Induction and Evaluation Of Arthritismentioning

confidence: 99%

“…Recent studies have demonstrated that the dominant immunogenic epitopes of some T cell-mediated experimental autoimmune diseases can be precisely defined by using disease inducing T cell clones as tools (Zamvile;a/,, 1986;van Eden e^o/,, 1988), In adjuvant arthritis (AA), a model of autoimmune arthritis inducible in certain strains of rats such as in Lewis rats, by heatkilled Mycobacterium tuberculosis (Pearson, 1956;1964;Taurog, Argentieri & McReynolds, 1988), a 65-kD mycobacterial heat-shock protein (HSP) has been proposed to be involved in the pathogenesis of AA (van Eden et al, 1988), Administration of the 65-kD HSP led to protection against AA and streptococcal cell-wall-induced arthritis in Lewis rats (van Eden et al, 1988;van den Broek et al, 1989;Billingham et al, 1990). A nonapeptide (Thr-Phe-Gly-Leu-Gln-Leu-Glu-Leu-Thr), representing amino acid sequence 180-188 ofthe 65-kD mycobacterial HSP, has been suggested to carry the critical epitope(s) for A A because of its ability to stimulate the arthritis-inducing T cell clone A2b as well as the arthritis-protective T cell clone A2c in vitro (Holoshitz, Matitiau & Cohen, 1984;Cohen et at., 1985;van Eden et al, 1988;, Based on these observations, it was suspected that immunization with the Correspondence: Dr X,-D, Yang, R-1056.…”

Section: Introductionmentioning

confidence: 99%

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Prevention of adjuvant arthritis in rats by a nonapeptide from the 65-kD mycobacterial heat-shock protein

Yang

Gasser

Feige

1990

Clinical and Experimental Immunology

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SUMMARYAdjuvant arthritis in Lewis rats is a model of T cell-mediated autoimmune arthritis resembling human rheumatoid arthritis, A nonapeptide from the 65-kD heat-shock protein of Mycobacterium bovis BCG, amino acid sequence 180-188, has been described to carry the dominant immunogenic epitope(s) for both arthritis-protective and arthritogenie T cell clones. Here we demonstrate that immunizations with the synthetic nonapeptide completely protected rats against adjuvant arthritis induced by M. tuberculosis. Interestingly, deletion of the N-teminal threonine of the nonapeptide resulted in loss ofthe protective activity, Pretreatments with the nonapeptide resulted in an immune response to the nonapeptide and to M. tuberculosis. After immunizations with the synthetic nonapeptide, only low titres of nonapeptide-specific antibodies were produced, whereas a significant cellular immune response to the nonapeptide was observed. In addition, the protection was transferable to naive rats by spleen T cells. These findings document the requirement of a T cellspecific immune response to the dominant epitope ofthe 65-kD mycobacterial heat-shock protein for the protection against adjuvant arthritis and suggest the feasibility of immune intervention in autoimmune arthritis through the use of synthetic peptides.

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[31] Adjuvant arthritis

Cited by 106 publications

References 28 publications

Potential role of heme oxygenase-1 in the progression of rat adjuvant arthritis

Potential role of heme oxygenase-1 in the progression of rat adjuvant arthritis

Up‐regulation of cyclooxygenase‐2 mRNA in the rat spinal cord following peripheral inflammation

Prevention of adjuvant arthritis in rats by a nonapeptide from the 65-kD mycobacterial heat-shock protein

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