Serum protein alterations in adjuvant-induced arthritis

Weimer, Henry E.; Wood, Fae D.; Pearson, Carl M.

doi:10.1139/o68-114

Cited by 27 publications

(9 citation statements)

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“…In the secondary inflammatory phase of adjuvant arthritis, the degree of swelling was much greater than the primary phase but the change in levels of APPs were less than would be predicted had levels of APPs been directly correlated to the degree of inflammation. The changes in levels of haptoglobin, seromucoid and caeruloplasmin were similar to results obtained by other researchers [17,26,27]. This lack of change, or down-regulation of response, during the secondary phase could be caused by a variety of factors: release of cytokine inhibitors, reduced release of cytokines or the liver synthesis of the proteins reaching a maximal level.…”

Section: Discussionsupporting

confidence: 88%

A simple inflammation model that distinguishes between the actions of anti-inflammatory and anti-rheumatic drugs

Lewis

Bishop

Aspinall

1998

Inflammation Research

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Section: Discussionsupporting

confidence: 88%

A simple inflammation model that distinguishes between the actions of anti-inflammatory and anti-rheumatic drugs

Lewis

Bishop

Aspinall

1998

Inflammation Research

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“…The major depression of SH level occurs during this phase, and those changes which occur during the acute phase are more moderate, and appear to be transitory. Other biochemical changes have been reported to occur in AA, including depressed serum albumin levels, raised fibrinogen and a-2-macroglobulins, and impaired liver microsomal oxidase activity (Lowe, 1964;Weimer, Wood, and Pearson, 1968;Beck and Whitehouse, 1973). All of these changes, however, are expressed during the initial acute inflammatory phase and can be induced by agents such as croton oil and carrageenan without leading to AA (Goldstein, Shemano, Demeo, and Beiler, 1967;Varsa-Handler, Handler, and Gordon, 1967;Glenn, Gray, and Kooyers, 1965).…”

Section: Discussionmentioning

confidence: 99%

Protein sulphydryl depression during adjuvant arthritis.

Lorber¹,

Leeb²,

Carroll³

et al. 1975

Annals of the Rheumatic Diseases

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. Protein sulphydryl depression during adjuvant arthritis. The changes in plasma protein sulphydryl level were measured during the course of adjuvant-induced arthritis in rats. Major depressions in the plasma sulphydryl level occurred at the onset of adjuvant disease, and the extent of the depression was related to the severity of the disease. Plasma sulphydryl levels remain unchanged when the systemic arthritis is suppressed by inclusion of a competing antigen in the adjuvant. Changes in sulphydryl content of the plasma were shown not to be due to weight loss or decrease in plasma protein level. Materials and methodsFor all experimental and control groups, 5 male Lewis strain rats (Microbiological Associates) weighing 150-250 g initially, were used. Adjuvant arthritis was induced by intradermal injection of 010 ml Freund's complete adjuvant into a foot pad of the left hind paw. The adjuvant was prepared by suspending Mycobacterium butyricum (Difco Laboratories) in paraffin oil (6-0 mg/ml).The arthritis score was used as an index of the severity of the AA and was determined by observation of the extent of swelling, lesions, and redness of each joint, including the tail, with scores of 0 to 4 being assigned to each joint. The maximum score for one animal was 20.Blood samples were collected into heparinized tubes by amputation of the tip of the tail. Plasma protein SH was determined radiochemically by addition of 0-1 ml plasma to 0-2 ml 203Hg p-chloromercuribenzene sulphonic acid (PCMBS, 1-18 mmol/l in 0 09 % NaCl), to a final volume of 1 5 ml with water followed by precipitation with 1-5 ml of 7 % trichloroacetic acid (TCA) and centrifugation.Precipitates were washed twice with 3-750% TCA, and protein bound 203Hg in the precipitates was counted in a well scintillation spectrometer. When larger sample volumes were available, serum sulphydryl levels were also measured by argentometric titration, and no significant differences were found. In those occasional samples which showed signs of haemolysis, corrections were made for heme protein SH in the plasma samples by determining (before TCA precipitation) the heme peak at 415 nm in both the plasma sample and an appropriately diluted haemolysate of cells from the same animal. The haemolysate was analysed for SH in the same manner as the

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“…Many changes occur in the blood during the development and onset of arthritis [1,5], an increase in serum lysosomal enzymes being one of these [6]. The latter, along with contributions from other altered serum components, probably facilitates and assures the development, severity and chronicity of adjuvant-induced disease.…”

Section: Introductionmentioning

confidence: 99%

A major contributory cause of arthritis in adjuvant-inoculated rats: Granulocytes

et al. 1977

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AbstraetThe predominant white ceil-type in circulating blood of normal rats is the lymphocyte. Granuloeytes increase in the circulating blood of adjuvant-inoculated rats; lymphocytes remain the same or increase slightly. Some drugs, like Cytosar | (cytarabine), inhibit granuioeyte increases primarily and inhibit arthritis development completely. Pretreatment of normal rats with cytarbine also inhibits the local inflammation caused by direct injections of M. butyrieum into hindpaws of rats. Pre-treatment of rats with M.butyrieum, causing granulocytes to increase in circulating blood, produces an exaggerated response to the subsequent inoculation ofM. butyricum directly into rats' paws.Injection of M. butyrieum in non-arthrltogenic vehicles (saline) does not produce the exaggerated response of granulocytes that occurs in response to injection in effective arthritogenic vehicles (mineral oil). Granulocytes are not increased greatly using the ineffective vehicle. Finally, lysates of either rat white cells (granulocytes) or platelets, both of which increase in adjuvant-inoculated rats, produce striking inflammatory reactions when inoculated locally into rats' hindpaws. The addition of non opsonized M. butyricum to granulocytes obtained from adjuvant-inoculated rats causes a significant increase in the release oflysosomal enzymes.From all these and other indirectly derived data, it is surmised that adjuvant inoculation produces a marked increase in granulocytes of circulating blood; as these increase with time, the 114. butyricum molecules or some constituent derived from them (as determined by the distribution of tritiated M. butyricum) arrive in joints and many other tissues, there reacting with granulocytes causing release of lysosomal constituents that produce the histopathology of adjuvant-disease. These results are discussed. IntroductionThe pathways and mechanisms for development of adjuvant-arthritis in the rat are unknown. Following inoculation of certain adjuvants (organism + appropriate vehicle)intradermally, rats develop a widespread disseminated disease, involving many organs -the appendages being only one manifestation of this

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Serum protein alterations in adjuvant-induced arthritis

Cited by 27 publications

References 0 publications

A simple inflammation model that distinguishes between the actions of anti-inflammatory and anti-rheumatic drugs

A simple inflammation model that distinguishes between the actions of anti-inflammatory and anti-rheumatic drugs

Protein sulphydryl depression during adjuvant arthritis.

A major contributory cause of arthritis in adjuvant-inoculated rats: Granulocytes

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