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Query: UMLS:C0003864 (arthritis)
 69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors describe the inhibiting action of mannitol after repeated administration of low subcutaneous doses in a number of experimental immunological models. For example, in the rat it produces a reduction of the secondary arthritis of Freund's adjuvant polyarthritis and also of the pleurisy due to Bordetella pertussis hypersensitivity. In the mouse it reduces the reaction of delayed hypersensitivity to sheep red cells. Its action is also marked against ovalbumin-induced active skin anaphylaxis in the albino guinea-pig and on IgE synthesis in the rat. Moreover, after several injections it produces a reduction of carbon phagocytosis in the mouse. At the doses at which the effect appeared, no action could be found on various models of acute non-immune inflammation, diuresis, blood pressure, hematocrit and protein and plasma sodium levels.
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PMID:Action of mannitol in various immunological experimental models. 22 21

In order to investigate arthritis-triggering, serologically cross-reactive antigens, sera from patients infected with arthritis-associated microbes, Salmonellae, Chlamydia trachomatis, and Sindbis-like alphavirus, were reacted against SDS-PAGE separated and immunoblotted Yersinia enterocolitica 0:3 antigens. These sera reacted with Yersinia to the same extent as did the control sera taken from patients with streptococcal, staphylococcal and Bordetella pertussis infections or from healthy blood donors. Moreover, the various sera produced different reactivity patterns, directed against several different antigens. Although sera from test subjects, as well as from controls including healthy individuals, recognized some Yersinia antigens, these patterns differed markedly from those recognized by sera taken from patients with Yersinia infection. Significantly, analysis of the reactivities against the different molecular weight antigen components of Yersinia revealed no dominant band or pattern which could thus have been defined as arthritis-associated.
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PMID:Serological cross-reactions against Yersinia enterocolitica in patients infected with other arthritis-associated microbes. 216 7

The formation of an air pouch in the subcutaneous tissues of a rat previously inoculated intradermally with Freund's mycobacterial adjuvant for the induction of arthritis, provokes a marked but transient inflammatory reaction in the cavity lining of the pouch. The dependence of this reaction on arthritis development was investigated. It was found that rats inoculated with mycobacterial adjuvant by subcutaneous or intraperitoneal injection failed to produce either a pouch reaction or develop arthritis. Intradermal injections of carrageenan, mycobacteria (M. tuberculosis in saline), Freund's incomplete adjuvant alone or containing Salmonella typhimurium lipopolysaccharide and Bordetella pertussis organisms or mycobacterial adjuvant containing egg albumin were also ineffective. Intradermal injections of type II collagen in Freund's incomplete adjuvant did induce arthritis but no pouch reaction; however, this could be elicited after direct challenge with antigen. Pretreatment of rats intraperitoneally with saline suspensions of mycobacteria or a moderate dose of cyclophosphamide prevented both the pouch reaction and arthritis developing to intradermal mycobacterial adjuvant. Pretreatment of rats with mycobacteria was without effect on type II collagen-induced arthritis. From the results of this study it would appear that the air pouch reaction and arthritis induced by adjuvant are directly associated. The inability of collagen to induce a similar reaction demonstrates a fundamental dissimilarity with mycobacterial adjuvant in its mechanism of production of arthritis.
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PMID:Polyarthritis and the air pouch reaction: dissimilarity of adjuvant and collagen models. 337 28

Chronic monoarticular allergic arthritis was induced in BALB/c mice using methylated BSA as antigen and Freund's complete adjuvant, together with Bordetella pertussis as a secondary adjuvant. The optimum conditions for induction of chronic persistent arthritis and the histological characteristics of the arthritic lesion are described. Both the synovitis and erosive progression of the arthritis could be suppressed by daily treatment with prednisolone (1-10 mg/kg) or dexamethasone (0.5-2.5 mg/kg) for 4 weeks commencing 2 weeks after the induction of arthritis. In contrast, daily treatment with the non-steroidal anti-inflammatory agents ibuprofen (50-100 mg/kg), flurbiprofen (1-9 mg/kg) or indomethacin (0.1-3 mg/kg) had no significant effect on either the synovitis or erosions as judged histologically. Synovial fluid differential leukocyte counts were altered by treatment with ibuprofen and indomethacin but not by flurbiprofen or the corticosteroids. The suppressive effect of the corticosteroids was not due to either suppression of antibody synthesis or alteration of the number of leukocytes in the peripheral circulation.
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PMID:Pharmacological studies of antigen-induced arthritis in BALB/c mice. I. Characterization of the arthritis and the effects of steroidal and non-steroidal anti-inflammatory agents. 375 51

In an attempt to produce a superior model of rheumatoid arthritis, experiments have been performed to investigate the ease of induction of experimental arthritis in marmosets by immunological means. Marmosets were sensitised with the following combinations of antigen and adjuvant: ovalbumin in Freund's complete adjuvant (FCA), ovalbumin in FCA + Bordetella pertussis, methylated-BSA in FCA + B. pertussis or human fibrin in FCA + B. pertussis, and subsequently injected with the corresponding antigen in saline into one knee joint. Animals receiving ovalbumin, with or without B. pertussis, produced only a weak transient monoarticular synovitis. Animals receiving Met-BSA + B. pertussis produced a chronic synovitis but only mild erosive changes were apparent even 21 weeks after intraarticular injection. Animals receiving human fibrin produced a transient monoarticular synovitis of moderate intensity. These results indicate that the marmoset offers no obvious advantages over the rabbit for the induction of experimental rheumatoid arthritis.
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PMID:Investigations into the induction of chronic experimental arthritis in the common marmoset (Callithrix jacchus). 662 24

Glycosaminoglycans such as heparin, heparan sulphate and dermatan sulphate, are distributed widely in the human body. Several glycosaminoglycans form part of the extracellular matrix and heparan sulphate is expressed on all eukaryotic surfaces. The identification of specific binding to different glycosaminoglycan molecules by bacteria (e.g., Helicobacter pylori, Bordetella pertussis and Chlamydia trachomatis), viruses (e.g., herpes simplex and dengue virus), and protozoa (e.g., Plasmodium and Leishmania), is therefore of great interest. Expression of glycosaminoglycan-binding proteins depends on growth and culture conditions in bacteria, and differs in various phases of parasite development. Glycosaminoglycan-binding microbial proteins may mediate adhesion of microbes to eukaryotic cells, which may be a primary mechanism in mucosal infections, and are also involved in secondary effects such as adhesion to cerebral endothelia in cerebral malaria or to synovial membranes in arthritis caused by Borrelia burgdorferi. It has been suggested that they may enhance intracellular survival in macrophages. Microbial binding of heparin may interfere with heparin-dependent growth factors. Whether or not glycosaminoglycan-binding proteins mediate invasion of epithelial cells is a matter of controversy. Heparin and other glycosaminoglycans may have potential uses as therapeutic agents in microbial infections and could form part of future vaccines against such infections.
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PMID:Glycosaminoglycan-binding microbial proteins in tissue adhesion and invasion: key events in microbial pathogenicity. 1033 89

A total of 100 poultry farms in northern and middle areas of Jordan were sampled to investigate the bacteria associated with airsacculitis in broiler chickens. Of 170 bacterial isolates, 88.2% were identified as Escherichia coli, 8.8% as Ornithobacterium rhinotracheale, and 3% as Bordetella avium. Fourteen serotypes of E. coli were identified among 66 typeable isolates and the remainder were untypeable. The most prevalent serotypes were O1, O8, and O78. The main serotype of O. rhinotracheale was serotype A. Experimental inoculation of O. rhinotracheale via intravenous, intratracheal, and intra-air sac routes resulted in growth retardation, thickening in the air sacs, arthritis, and liver necrosis. Reisolation of O. rhinotracheale from the air sacs, liver, trachea, heart, and spleen at day 7 postinoculation confirmed its role. In vitro susceptibility testing revealed that E. coli isolates were sensitive to gentamicin and colistin, O. rhinotracheale to tetracyline, and B. avium to most of the nine antibiotics examined.
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PMID:Studies on the bacterial etiology of airsacculitis of broilers in northern and middle Jordan with special reference to Escherichia coli, Ornithobacterium rhinotracheale, and Bordetella avium. 1224 24

The effects of ferric-sorbitol-citrate and ferric-citrate on the severity of experimental arthritis, TNF-alpha secretion and the immune status were examined in mice. Arthritis was induced by footpad injection of methylated BSA and intraperitoneal injection of Bordetella pertussis. Joint and footpad swelling were measured weekly by a caliper. TNF-alpha serum levels were measured by ELISA. The immune status was determined by the response of mouse lymphocytes to ConA in vitro and by the antigen-presenting cell assay. Experimental arthritis was aggravated by ferric-citrate, whereas ferric-sorbitol-citrate did not promote it. If applied to normal (non-arthritic) mice three times a week for 4 weeks, ferric-sorbitol-citrate stimulated isolated splenocytes to increase production of TNF-alpha, the function of antigen-presenting cells and lymphocyte proliferation in response to ConA in vitro. TNF-alpha production by cultured splenocytes was also stimulated. In mice with antigen-induced arthritis, iron compounds did not additionally stimulate TNF-alpha production. Thus, we have shown that ferric-sorbitol-citrate stimulated TNF-alpha production, antigen-presenting cell activity and cellular immune response. Development of antigen-induced arthritis and TNF-alpha production in arthritic mice were not stimulated.
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PMID:Differing effects of two iron compounds on experimental arthritis, TNF-alpha levels and immune response in mice. 1463 25

Antigen induced arthritis is a unilateral T-cell driven model caused by direct injection of an antigen into the knee joint of a FCA preimmunized animal. The chronicity is determined by antigen retention in avascular structures of the joint through charge mediated binding or antibody mediated trapping. Cationicity of the antigen is a prerequisite in this model in the mouse and commercial mBSA is a suitable antigen. Cartilage erosive character is strongly enhanced in the presence of marked antibody titer. Concomitant boosting of the immune response with Bordetella pertussis adds to this. T-cell mediated flares can be induced by local or systemic rechallenge with low dose antigen, and display a strong erosive phenotype.
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PMID:Murine antigen-induced arthritis. 1798 53

Extrinsic allergic alveolitis (hypersensitivity pneumonitis), especially humidifier lung, has been more frequently diagnosed over the last decades, whereas farmer's lung has decreased over the same time period. Today two types of the chronic course of extrinsic allergic alveolitis can be distinguished. The recurrent chronic course with a good prognosis may be differentiated from the insidious course with a poor prognosis by means of different histological patterns (UIP, NSIP, BOOP pattern). The characteristic neutrophilic infiltration of the lung in the insidious course cannot be detected by bronchoalveolar lavage (BAL) methods. Furthermore, lymphocytosis in the BAL can be absent or present at a low level. The CD4/CD8 ratio is not always decreased and may be normal or even increased in these insidious cases with a poor prognosis. Granulomas in the lung tissue, however, point to a good prognosis. In the diagnostic work-up of machine operator's and humidifier lung, it is advisable not only to look for serum antibodies against bacteria and molds but also for rapid growing mycobacteria in a sample of machine or humidifier water. IgM and IgG rheumatoid factors occur frequently in allergic alveolitis, especially in humidifier lung. The patients, however, do not suffer from arthritis. The IgM rheumatoid factor may simulate IgM antibodies against numerous infectious agents (e. g., Bordetella pertussis or Mycoplasma pneumoniae). Taking this phenomenon into account may improve the current differential diagnosis of allergic alveolitis.
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PMID:[Recent advances in extrinsic allergic alveolitis]. 1804 Sep 29


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