Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003864 (arthritis)
 69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prolonged oral treatment (up to 410 days) of rabbits with D-penicillamine at a dose of 15 mg/kg body weight commencing either before or after immunization and the onset of arthritis, diminished and eventually abolished the delayed hypersensitivity response to intradermally administered tuberculin PPD. The 48 h cutaneous hypersensitivity response to the immunizing antigen (ovalbumin) was also significantly reduced, as was the inhibition of leucotye migration by ovalbumin. Cutaneous Arthus reactivity to ovalbumin was unaffected by D-penicillamine treatment. D-penicillamine treatment of normal rabbits was also found to increase the phagocytic index of the reticuloendothelial system as measured by carbon clearance.
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PMID:The effects of oral D-penicillamine treatment on experimental arthritis and the associated immune response in rabbits. II. The effects on cellular parameters. 68 Jul 99

An experiment was designed to compare the efficiency of lymph node injection for the induction of adjuvant arthritis (AA) with that of conventional footpad injection in the rat. Quantitative studies revealed that the minimal dose required for induction of AA by the lymph node route is one fifth of that by the footpad route. Thus, the lymph node route was found to be more efficient than the footpad method in terms of higher incidence and earlier onset of AA. PPD in Freund's incomplete adjuvant was able to produce tuberculin sensitization in the rat. The lymph node route again proved to be superior in terms of consistent appearance of the 24-hour reaction on days 8 and 14 and prolongation of the skin reaction over 48 h. These findings show that the lymph node method is so efficient in the rat that it will be especially useful for the trial induction of AA with various materials of unknown potency as well as for production of delayed hypersensitivity. In addition, this injection method appears to be a simple and efficient technique for assay of other immunological reactions.
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PMID:Reevaluation of inguinal lymph node injection for production of adjuvant arthritis in the rat. 81 81

Bacterial cell walls from Str. bovis, Str. lactis, Str. mutans, Str. thermophilus, Str. salivarius, and Str. pyogenes were able to produce polyarthritis in rats but Str. faecalis cell walls were nonarthritogenic. S. aureus cell walls produced extremely severe disease. It was also shown that cell walls from S. epidermidis, B. megaterium, and M. lysodeikticus were nonarthritogenic. A close correlation was observed between development of arthritis and the delayed hypersensitivity to bacterial peptidoglycans but not with the PPD hypersensitivity. It was suggested that the adjuvanticity of bacterial cell walls is needed to induce the disease and that arthritogenicity requires a specific antigen in addition to the presence of an adjuvant-inducing agent.
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PMID:Arthritogenicity in rats of cell walls from several streptococci staphylococci and two other bacteria. 81 36

Two derivatives of wax D, one possessing immunogenicity and the other adjuvant activity, were tested for the possible role in the induction of adjuvant arthritis (AA) in rats. The former, a water-soluble arthritogenic and immunogenic component (WAC), in incomplete Freund's adjuvant, was able to induce delayed hypersensitivity (DH) and mild AA, but failed to function as an adjuvant in rats. The latter, an acetylated wax D (AD) and its subfraction, AD6, did exert adjuvant activity, but were free from immunogenicity and arthritogenicity. The addition of AD or AD6 to the WAC in incomplete Freund's adjuvant, when injected into inguinal lymph nodes, resulted in the production of severe AA with high incidence. Other adjuvants such as pertussis vaccine and lipopolysaccharide could not replace AD6; they failed to enhance AA when combined with the WAC. Also, other mycobacterial antigen, PPD, could not replace wax D-derived WAC; it did not induce AA when coupled with AD6, although it did induce DH to PPD.
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PMID:Synergism of immunogenic and adjuvant-active components of mycobacterial wax D in the induction of adjuvant arthritis. 82 21

Most of wax D (peptidoglycolipid) used here appeared to be ineffective for production of arthritis when given in a water-in-oil emulsion, while the same wax D in squalane was very effective for production of arthritis. Arlacel A as an emulsifier appeared to suppress the arthritogenicity of wax D in squalane, probably through some interaction with the arthritogenic portion of wax D. Poly 1:C seemed to remarkedly enhance the arthritogenicity of wax D, even in water-in-oil emulsion. Acetylated wax D and cord factor (trehalsoe-dimycolate) were much less effective than poly 1:C. Delayed skin hypersensitivity to PPD, peptidoglycan and poly 1:C was also remarkedly affected by oil composition. However, there was no correlation between these delayed hypersensitivities and development of arthritis.
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PMID:Arthritogenicity of wax D from various mycobacteria related to oil vehicle composition and to the combination with poly I:C, cord factor and acetylated wax D. 85 4

Lymphocyte transformation to various mitogens and antogens was studied in selected patients with systemic lupus erythematosus. These patients were selected because they had taken no drug other than low-dose aspirin for 2 months prior to presentation. An impaired transformation response to the mitogens phytohemagglutinin and pokeweed was found. There was no impairment in the response to PPD and Candida. The impaired mitogen response, which could not be corrected using purified, warm-washed, and warm-cultured T lymphocytes, seemed to be a corollary of disease activity.
Arthritis Rheum
PMID:Lymphocyte responsiveness in systemic lupus erythematosus. 108 54

There is no group proof of long acting antirheumatics (LAA) in laboratory animal models, and it is not to be expected without an identical rheumatoid arthritis model in animals and with regard to the heterogeneity of LAA. However, LAA are to be detected according to D-penicillamine-like, levamisol-like etc. actions, which can be disclosed in the adjuvant arthritis as well as in the B. pertussis-vaccine pleuritis in rats the latter model best by including parameters of inflammatory exudate cells. Modification of the models or of model parameters (BCG-sensibilization, PPD reaction, vasoreactivity, RNA content of exudate cells, SH groups, copper zinc) are hardly advantageous, contrarily to dosage. Other models, among them paw edemas, do not permit sufficient testing of LAA, even not the methyl-albumin mice paw edema. There is no problem of pharmacologically separating LAA actions from nonsteroidal or steroidal antiphlogistics actions.
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PMID:[The testing of long-term antirheumatics in animals]. 244 99

Oral administration of spirogermanium (Sg), inhibits the development of immune-mediated hindpaw inflammation in the rat model of adjuvant arthritis (AA) and DTH responses to PPD (30 mg/kg/day). A similar dosing protocol inhibits hindleg paralysis in experimental autoimmune encephalomyelitis (EAE). The spleens of these animals and those of normal rats contain radiation resistant (2000 R) non-specific suppressor cells (SC) which bear some similarity to those generated following total lymphoid irradiation (TLI). These cells do not appear to be mature T cells, they are partially adherent to plastic, sephadex G10 and nylon wool, insensitive to indomethacin and are enriched in a 1.07 g/ml fraction of a Percoll density gradient.
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PMID:Inhibition of autoimmune disease and the generation of suppressor cells by spirogermanium: a biological profile similar to total lymphoid irradiation. 252 42

The suppressor effect of synovial fluid (SF) T8 cells and blood T8 cells on the pokeweed mitogen (PWM)-induced T4 cell-dependent immunoglobulin production of autologous blood B cells was studied in nine patients with chronic rheumatic diseases (six patients with rheumatoid arthritis (RA), one patient with juvenile RA, and two patients with other forms of chronic arthritis). The suppressor effect of SF T8 cells was of the same magnitude as that of equal numbers of blood T8 cells from patients and healthy controls. However, the relative number of T8 cells was higher among SF T cells than among blood T cells in several cases. Good synovial T8 cell suppression was also demonstrated in coculture experiments where SF T4 cells and B cells were used. In PPD (purified protein derivative of tuberculin)-stimulated cultures the suppressor effect of SF T8 cells as well as of blood T8 cells from patients and controls was lower than it was in PWM-stimulated cultures. In most patients SF T4 cells showed a much better PWM-induced helper function than did non-fractionated SF T cells. Thus the poor PWM induced helper effect of non fractionated synovial T cells was in some cases mainly due to the suppressor effect of T8 cells, whereas in some cases there was also a deficient helper function of synovial T4 cells.
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PMID:Immunoregulatory function of T8 and T4 cells from synovial fluid and blood of patients with rheumatoid arthritis or other forms of chronic arthritis. 294 75

T-cell lines were established from the lymph node cells of syngeneic Louvain (LOU) rats previously immunized with native chick type II collagen (CII) emulsified in incomplete Freund's adjuvant. The CII lines proliferated in vitro to type II collagen but not to type I collagen, ovalbumin (OV), or PPD. Control lines, developed from LOU rats immunized with OV emulsified in complete Freund's adjuvant, were OV specific because they did not respond to other antigens in vitro. CII line cells could adoptively transfer delayed-type hypersensitivity (DTH) but did not induce IgG antibody production to collagen. Moreover, the intravenous administration of 2 X 10(7) CII line cells prevented the subsequent induction of collagen arthritis following immunization and suppressed DTH to collagen without affecting antibody responses in the recipients. Spleen cells, but not sera, from these resistant rats decreased CII line reactivity in vitro. OV or irradiated CII lines had no effect on clinical or immunologic parameters in this model. These findings demonstrate protection from arthritis afforded by T-cell line transfer and suggest that the phenomenon results from down-regulation of the recipients' cellular immunity to collagen.
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PMID:Attenuation of collagen arthritis and modulation of delayed-type hypersensitivity by type II collagen reactive T-cell lines. 349 39


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