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

Water-soluble substances have been extracted from two strains of Mycobacterium tuberculosis var. hominis: the native hydrosoluble part (polysaccharide and peptidoglycan), a substance in which the polysaccharide moiety is less abundant than in the latter, the acetylated peptidoglycan and, finally a tetrasaccharide-heptapeptide. All four types of substances, when they were injected together with Freund's incomplete adjuvant, exerted an adjuvant effect on the production of delayed-type hypersensitivity to ovalbumin in the guinea pig and on the production of anti-influenza virus antibodies in the rabbit. Injected intravenously in the mouse, they increased the number of antibody-producing cells in the spleen and enhanced the graft versus host reaction; no effect was seen on the phagocytic activity of the reticulo-endothelial system. By contrast with wax D, the water-soluble substances were devoid of arthritis-inducing activity in the rat. Altogether, these water-soluble substances seem to be endowed with at least some of the adjuvant activities of Freund's complete adjuvant and some of the immunostimulant activities of a live Mycobacterium like BCG.
 ...
PMID:Adjuvant and immunostimulating activities of water-soluble substances extracted from Mycobacterium tuberculosis (var. hominis). 0 66

Monosodium urate monohydrate (MSUM) is a potent activator of the complement system as measured by electrophoretic conversion of beta1C to beta1A. Activation of C3 in human serum by MSUM is both time- and dose-dependent. The sensitivity of the assay allows detection of C3 activation by as little as 0.2 mg/ml of MSUM. It was observed that C3 activation is calcium dependent and elimination by both EDTA and EGTA, a finding that demonstrated the major role of the classic pathway of complement activation. Excess calcium or magnesium alone inhibited C3 activation by MSUM in accord with the inhibitory effect of these cations on sensitized sheep cell hemolysis by complement. Heating of MSUM at 200 degrees C for 2 hours removes the water of crystallization such that heated crystals may no longer be considered MSUM. Such treatment has a variable effect on C3 activation. Of the crystals and other material studied, only zymosan was more potent than MSUM in activating C3. Calcium prophosphate dihydrate and hydroxyapatite activated significant amounts of C3. Asbestos, glass wool, or a variety of microcrystalline steroids activated little or no C3.
Arthritis Rheum 1979 Jun
PMID:C3 activation by monosodium urate monohydrate and other crystalline material. 11 Mar 37

Germfree F344 rats developed severe arthritis with 100% incidence after a single intradermal inection of either squalane containing 0.5 mg of heat-killed Mycobacterium bovis BCG or a water-in-oil emulsion containing 0.2 mg of peptidoglycan derived from Staphylococcus epidermidis. Conventional F344 rats developed less-severe arthritis with 20% incidence for heat-killed BCG and 0% incidence for peptidoglycan. Specific-pathogen-free rats showed an intermediate susceptibility between germfree and conventional rats. Interestingly, both unimmunized specific-pathogen-free and conventional rats. but not unimmunized germfree rats, showed weak delayed-type hypersensitivity reactions to peptidoglycans derived from either S. epidermidis or Lactobacillus plantarum, suggesting that a bacterial flora may furnish a stimulus for induction of cell-mediated immunity to ubiquitous bacterial peptidoglycans. It is thus possible that although a bacterial flora is not necessary for development of adjuvant arthritis, it may have some suppressive effect on the development of the disease in specific-pathogen-free and conventional F344 rats, possibly through modulation of the immune response.
 ...
PMID:Susceptibility to adjuvant-induced arthritis among germfree, specific-pathogen-free, and conventional rats. 16 Aug 88

Phenol-water extracted rheumatoid synovial fluids and synovial fluid leukocytes contain an antigen immunologically identical to the Proprionibacterium group bacteria. The antigen was identified by counter-immunoelectrophoresis in 70% of rheumatoid synovial fluid leukocyte pellets and in 60% of rheumatoid synovial fluids. It was also present in 6% of nonrheumatoid fluids and in 22% of nonrheumatoid inflammatory fluid leukocytes. Antigen was not detectable in synovial samples before extraction. Synovial and bacterial antigens were further purified by proteolytic digestion and Sepharose 4B column chromatography. Biochemical and enzymatic studies of bacterial and synovial antigens were similar and consistent with a high molecular weight polysaccharide. Serum antibody to bacterial and synovial antigens was significantly less frequent in rheumatoid sera than in normal controls. The significance of demonstrating a bacterial polysaccharide primarily in rheumatoid synovial effusions is discussed.
Arthritis Rheum 1979 Sep
PMID:Antigenic bacterial polysaccharide in rheumatoid synovial effusions. 31 93

Skin biopsies of uniform location and surface area (7 mm diameter) were obtained from the extensor aspect of the forearm of 147 patients with progressive systemic sclerosis (PSS) (107 with diffuse scleroderma, 40 with the CREST syndrome variant) and 58 individuals with normal skin. After careful removal of all subcutaneous fatty tissue, the skin cores were weighed and their water and hydroxyproline content determined. Despite recent claims to the contrary, it was found that there is a marked and highly significant increase in the thickness of the skin during the indurative phase of PSS, and that this is associated with a proportionate increase in total dermal collagen content. A similar degree of thickening was found in the skin of patients with eosinophilic fasciitis and acromegaly. A close correlation was observed between clinical estimation of the degree of skin thickening and the weight of the skin biopsy cores. Change in the weight of skin cores was observed during the course of illness of the patients with PSS and may serve as a useful measurement of alteration in the degree of skin thickening.
Arthritis Rheum 1979 Feb
PMID:Skin thickness and collagen content in progressive systemic sclerosis and localized scleroderma. 42 Jul 6

In patients with rheumatoid arthritis, as well as in persons with other kinds of synovitis, proteins enter the knee joint more rapidly than in normal individuals (P less than 0.001). The rheumatoid synovium, however, is less permeable to small molecules (tritiated water, P less than 0.02; urate, P less than 0.05; and glucose, P less than 0.002) than is the normal joint lining. This difference is explained if rheumatoid microvascular changes enhance synovial permeability to proteins while coexisting interstitial changes diminish synovial permeability to smaller molecules.
Arthritis Rheum 1979 Jul
PMID:Synovial permeability in rheumatoid arthritis. 45 97

Lewis rats developed polyarthritis after a single injection of a water-in-oil emulsion containing various peptidoglycans (PGs) derived from Lactobacillus plantarum. A copolymer of polyriboinosinic acid and polyribocytidylic acid markedly potentiated the arthritogenicity of these PGs. The synthetic adjuvants N-acetylmuramyl-L-alanyl-D-isoglutamine (MurNAc-L-Ala-D-isoGln) and MurNAc-L-Ala-D-Gln were non-arthritogenic, but they did produce severe arthritis when mixed in a water-in-oil emulsion with a copolymer of polyriboinosinic acid and polyribocytidylic acid. Substitution of either L-isoGln or D-isoAsn for the D-isoGln in the MurNAc-L-Ala-D-isoGln markedly reduced its capacity to induce the disease. Taken together with the results of skin testing against various PGs and MurNAc-L-Ala-D-isoGln in the diseased rats, the present results suggest that (i) a minimal essential structure required for development of polyarthritis is related to a larger molecule than either MurNAc-L-Ala-D-isoGln or a monomer of PG, probably to a dimer of PG, and (ii) an antigenic determinant(s) for the delayed-type skin hypersensitivity to PGs exists on a common structure shared among these PGs, possibly somewhere on a monomer of PG not on N-acetylmuramyl peptides.
 ...
PMID:Synergistic effect of polyriboinosinic acid:polyribocytidylic acid and either bacterial peptidoglycans or synthetic N-acetylmuramyl peptides on production of adjuvant-induced arthritis in rats. 54 92

A number of purified cell walls of various gram-positive bacteria had arthritogenic activity in the rat. The water-soluble adjuvant-active component(s), which were isolated from some of these cell walls by utilizing a peptidoglycan-degrading enzyme, did produce severe adjuvant arthritis. However, the components obtained by digestion with glycan-degrading enzymes failed to produce arthritis. Thus, the present finding indicates the importance of a peptidoglycan portion, especially its intact glycan chain, for induction of adjuvant arthritis.
 ...
PMID:Induction of adjuvant arthritis in the rat by various bacterial cell walls and their water-soluble components. 77 38

In order to explore a possible role of the arabinogalactin (AG) portion of the water-soluble arthritogenic component (WAC) from M. tuberculosis wax D for induction of adjuvant arthritis (AA) in the rat, this component was digested with an AG-degrading enzyme. The enzyme-digested WAC was able to produce AA. The severity of AA was almost comparable to that of the nondigested WAC. This finding suggests that the AG portion of the WAC does not seem to be essential for AA induction and indirectly points the importance of the peptidoglycan portion.
 ...
PMID:Effect of degradation of the arabinogalactan portionof a water-soluble component from M. tuberculosis wax D on polyarthritis induction in the rat. 81 82

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.
 ...
PMID:Synergism of immunogenic and adjuvant-active components of mycobacterial wax D in the induction of adjuvant arthritis. 82 21


1 2 3 4 5 6 7 8 9 10 Next >>