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)

Sera from patients with active systemic lupus erythematosus caused the retention of the radioactively labeled synthetic polynucleotide 14C-dAT on cellulose nitrate filters. The amount of 14C-dAT bound correlated with the presence of hypocomplementemia and active renal disease. Sera containing only anti-single-stranded DNA antibodies did not bind 14C-dAT but did bind 125I DNA from E coli that had been prefiltered to remove ssDNA contamination. Inhibition experiments also indicated the presence of antigenic differences between 14C-dAT and prefiltered 125I-E coli DNA. The data suggest that dAT carries one of the major antigenic specificities for antinative DNA antibodies in SLE, and that cellulose nitrate filtration fails to remove a significant proportion of contaminating single-stranded DNA determinants in non-synthetic DNA.
Arthritis Rheum
PMID:Antibodies to dAT detected by membrane filtration. 108 27

The crystal induced chemotactic factor (CCF) is a protein released by human neutrophils (PMN-CCF) that phagocytize monosodium urate or calcium pyrophosphate crystals. This protein has been thought to play an important role in crystal induced arthritis. In the present report, a mouse hybridoma cell line A2900C2.12 which specifically secretes monoclonal antibody (MAb) to CCF has been developed. The antibody secreted by the cell line is mostly IgG2b and positive for both the light chains kappa and lambda. The MAb has been purified by affinity chromatography using a protein-A column. The purified MAb was found to be over 95% pure based on the results from SDS-PAGE. The MAb has been used to demonstrate that a leukotactic protein is released from polymorphonuclear leukocytes (PMN) and promyelocytic HL-60 cells in response to a phagocytic or degranulating stimuli such as monosodium urate crystals or N-formyl-Met-Leu-Phe (FMLP), respectively. "Western blots" and silver nitrate staining of the purified leukotactic protein from PMNs and HL-60 cells show that these proteins have the same immunodeterminant site(s) and both appear to have a molecular weight (m.w.) of about 15,000. A simple purification protocol including immunoaffinity high pressure liquid chromatography (HPLC) has been described for purifying chemotactic proteins with the same antigenic determinant as the PMN-CCF.
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PMID:Monoclonal antibody to the crystal induced chemotactic factor from human neutrophils detects similar immunoreactive and biologically active protein in promyelocytic HL-60 cells. 274 87

Analgesic and antipyretic effects of proglumetacin maleate (PGM), a new indomethacin (IND) derivative, were investigated in comparison with those of IND on an equimolar-dose basis. The suppression of phenylquinone-induced writhing in mice by PGM was about 0.8 and 2 times as potent as that by IND when given 1 and 4 hr before the phenylquinone injection, respectively. The analgesic activity of PGM in rat silver nitrate arthritis was about 1.5 times more potent than that of IND. PGM was slightly less active in rat adjuvant arthritic pain than IND. On the other hand, PGM provoked a dose-dependent antipyretic effect on the yeast-induced fever in rats within the dose range without affecting the normal body temperature. Furthermore, PGM showed a significant antipyretic effect on LPS-febrile rabbits. Generally, the antipyretic effect of PGM was moderate as compared with that of IND. These analgesic and antipyretic actions of orally administered PGM may be mainly due to its active metabolite, IND. The above results indicate that PGM may be useful for inflammatory diseases associated with pain and/or fever.
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PMID:[Pharmacological studies on proglumetacin maleate, a new non-steroidal anti-inflammatory drug. (2). Analgesic and antipyretic effects]. 349 Apr 20

An asaccharolytic, gram-negative, oxidase-positive diplococcus was isolated on Martin-Lewis medium from the cervix of a patient attending an arthritis clinic at Seattle Public Health Hospital, Seattle, Wash. This strain, NRL 32165, did not produce detectable acid from glucose, maltose, sucrose, fructose, mannitol, or lactose in either cystine Trypticase agar (BBL Microbiology Systems, Cockeysville, Md.) or modified oxidation-fermentation medium and was identified presumptively as a glucose-negative Neisseria gonorrhoeae strain, but was identified later as Neisseria cinerea on the basis of its biochemical reactions. Nitrate was not reduced, nitrite (0.001%, wt/vol) was reduced, and polysaccharide was not produced from sucrose. Proline, arginine, and cystine-cysteine were required for growth on defined medium. Strain NRL 32165 did not react with antigonococcal protein I monoclonal antibodies and did not produce immunoglobulin A protease. In DNA:DNA homology studies with N. gonorrhoeae NRL 8038 (F62) and N. cinerea type strain NRL 30003, strain NRL 32165 showed 95% homology relative to N. cinerea and 44% homology relative to N. gonorrhoeae. Thus, the identity of strain NRL 32165 was confirmed as N. cinerea (von Lingelsheim 1906) Murray 1939. Of all Neisseria spp., N. cinerea is most likely to be misidentified as a glucose-negative N. gonorrhoeae strain.
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PMID:Characterization of Neisseria cinerea, a nonpathogenic species isolated on Martin-Lewis medium selective for pathogenic Neisseria spp. 636 Oct 62

Anti-inflammatory, analgesic, and anti-pyretic activities of orally administered etofenamate, the diethylene glycol ester of flufenamic acid, were investigated in experimental animals. Against acetic acid-induced vascular permeability in mice and ultra-violet light-induced erythema in guinea pigs, etofenamate produced a dose related inhibition at doses of 40--320 mg/kg and 5--20 mg/kg, respectively. In rats, felt-pellet-induced granuloma formation and adjuvant-induced arthritis were significantly inhibited by repeated administration of etofenamate at doses of 20 mg/kg/day for 5 days and 40 mg/kg/day for 21 days, respectively. Etofenamate showed an inhibitory activity on the squeak response caused by flexing and extending the silver nitrate-induced arthritic joint in rats; and it produced a dose related anti-writhing activity at doses of 50--300 mg/kg and 10--80 mg/kg in mice and rats, respectively, in the acetic acid-induced writhing test. Etofenamate showed a significant anti-pyretic activity at doses of 0.2 mg/kg or more. These potencies of etofenamate were 0.5 to 1.6 times those of flufenamic acid. In particular, the anti-erythema, anti-arthritis, and anti-pyretic activities of etofenamate were approximately equivalent to or superior to those of flufenamic acid. From these results, it was suggested that etofenamate given orally, like other non-steroidal anti-inflammatory drugs, showed anti-inflammatory, analgesic, and anti-pyretic activities in experimental animals.
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PMID:[Anti-inflammatory, analgesic and anti-pyretic activities of a non-steroidal anti-inflammatory drug, etofenamate, in experimental animals]. 698 82

Plasma protein profiles were investigated electrophoretically in rats with aminonucleoside-induced glomerular damage, uranyl-nitrate-induced tubular damage, phalloidin-induced hepatocyte membrane damage, adjuvant arthritis as a model of chronic inflammation, and phenyl isothiocyanate pleurisy as a model of acute inflammation. Characteristic profiles were observed for each experimental disease, and their development and seriousness could be evaluated. Similar studies are already routinely used in clinical investigations of human plasma.
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PMID:Differentiation of various experimentally-induced patholgical processes in Wistar rats by serum protein electrophoresis using cellulose-acetate membranes. 743 26

MRL-lpr/lpr mice spontaneously develop various manifestations of autoimmunity including an inflammatory arthropathy and immune complex glomerulonephritis. This study examines the role of nitric oxide, a molecule with proinflammatory actions, in the pathogenesis of MRL-lpr/lpr autoimmune disease. MRL-lpr/lpr mice excreted more urinary nitrite/nitrate (an in vivo marker of nitric oxide production) than did mice of normal strains and MRL-(+/+) and B6-lpr/lpr congenic strains. In addition, MRL-lpr/lpr peritoneal macrophages had an enhanced capacity to produce nitric oxide in vitro as well as increased nitric oxide synthase activity, and certain tissues from MRL-lpr/lpr mice had increased expression of inducible nitric oxide synthase (NOS) mRNA and increased amounts of material immunoreactive for inducible NOS. Oral administration of NG-monomethyl-L-arginine, a nitric oxide synthase inhibitor, prevented the development of glomerulonephritis and reduced the intensity of inflammatory arthritis in MRL-lpr/lpr mice. By using interspecific backcross mice, the gene for inducible NOS (Nosi) was mapped to mouse chromosome 11. This chromosomal localization was different from those loci that we have previously demonstrated to be linked to enhanced susceptibility to renal disease in an MRL-lpr/lpr cross. However, the chromosomal location of the NOS gene was consistent with an insulin-dependent diabetes locus identified in an analysis of nonobese diabetic (NOD) mice. These results suggest that elevated nitric oxide production could be important in the pathogenesis of autoimmunity, and that treatments to block the production of nitric oxide or block its effects might be valuable therapeutically.
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PMID:The role of nitric oxide in the pathogenesis of spontaneous murine autoimmune disease: increased nitric oxide production and nitric oxide synthase expression in MRL-lpr/lpr mice, and reduction of spontaneous glomerulonephritis and arthritis by orally administered NG-monomethyl-L-arginine. 750 9

The murine model of Lyme disease was used to determine the role of inflammatory induced nitric oxide (NO) during infection by the spirochete Borrelia burgdorferi. The outer surface lipoproteins of B. burgdorferi are potent stimulators of inflammatory cytokines and NO production by cultured macrophages in vitro. The addition of NO to cultures of B. burgdorferi prevents growth, suggesting a protective role of NO for the infected host. NO is also a crucial effector in some models of arthritis. Therefore, the involvement of NO in controlling B. burgdorferi infection and its participation in pathological development of arthritis were investigated. Both mildly arthritic (BALB/c) and severely arthritic (C3H/HeJ) strains of mice systemically produced high levels of NO 1 week after infection with B. burgdorferi, as determined by urinary nitrate. NO production remained high throughout the infection in BALB/c mice, while in C3H/HeJ mice NO production returned rapidly to uninfected levels. The in vivo inhibitor of the NO synthase enzyme NG-L-monomethyl arginine (LMMA) was given to mice to investigate whether decreasing NO production would alter the course of disease. LMMA effectively blocked NO production in infected mice; however, there was no significant difference in arthritis development, spirochete infection of tissues, or production of specific antibody in LMMA-treated mice. These results indicate that B. burgdorferi is able to persist in the host even in the presence of high levels of NO. Furthermore, NO is not involved in the control of spirochete infection of tissues, nor is it involved in the development of arthritis. The potent activity of NO against intracellular pathogens and the in vivo resistance of B. burgdorferi to NO suggest that this organism is not located in an intracellular compartment during an essential portion of its infection of the mammalian host.
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PMID:Nitric oxide production during murine Lyme disease: lack of involvement in host resistance or pathology. 755 96

Nitric oxide (NO) is an important inflammatory mediator in nonhuman animal models of rheumatoid arthritis (RA). The purpose of the present study was to determine whether blood mononuclear cells from patients with active RA (as compared to control subjects) have higher levels of NO synthase type 2 (NOS2) and produce more NO in vitro. Leukocytes from 25 RA patients and 20 normal subjects were examined. Arthritis activity was assessed by tender and swollen joint counts, duration of morning stiffness, patient assessment of pain, physician and patient global assessment of disease activity, the modified Stanford Health Assessment Questionnaire, and by blood levels of acute phase reactants. Blood mononuclear cell NOS enzyme activity/antigen content and nitrite/nitrate formation in vitro were measured. Blood mononuclear cells from RA patients had increased NOS activity and increased NOS2 antigen content as compared to those from normal subjects, and responded to interferon-gamma with increased NOS expression and nitrite/nitrate production in vitro. NOS activity of freshly isolated blood mononuclear cells correlated significantly with disease activity, as assessed by render and swollen joint counts. Our results demonstrate that patients with RA have systemic activation for NOS2 expression, and that the degree of activation correlates with disease activity. Increased NOS2 expression and NO generation may be important in the pathogenesis of RA.
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PMID:Increased expression of blood mononuclear cell nitric oxide synthase type 2 in rheumatoid arthritis patients. 906 35

We have investigated the temporal relationship among proinflammatory cytokine expression, nitric oxide (NO) production and joint inflammation in the acute phase of bacterial cell wall-derived peptidoglycan polysaccharide (PG/PS)-induced arthritis. Acute joint inflammation was induced in female LEW/N rats by a single intraperitoneal injection of PG/PS. Arthritis index and paw volume were quantified and joint histopathology was evaluated during acute joint inflammation (0-10 days). Tumor necrosis factor (TNF), interleukin-1 (IL-1) and interleukin-6 (IL-6) were determined by bioassay whereas nitric oxide (NO) was quantified by measuring serum nitrate/nitrite levels via the Griess procedure. We found that serum levels of TNF and serum IL-1 preceded the increase in IL-6 and NO production. Furthermore, the production of these proinflammatory cytokines and NO preceded bone erosion and osteoclast activity. Erosion of subchondral bone preceded pannus formation and cellular synovitis in the acute phase of PG/PS-induced arthritis. The temporal expression of TNF, IL-1, IL-6 and NO suggest a cascade of inflammatory mediators in which monocytes and macrophages respond to PG/PS with enhanced synthesis of TNF and IL-1, which may in turn promote the synthesis of IL-6 and NO. We postulate that one or more of these inflammatory events are responsible for initiating the subchondral bone erosion observed in acute joint inflammation.
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PMID:Cytokine and nitric oxide production in the acute phase of bacterial cell wall-induced arthritis. 917 27


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