Chemical mediators of inflammation in acute gouty arthritis

Kellermeyer, Robert W.; Naff, George B.

doi:10.1002/art.1780180721

Cited by 29 publications

(13 citation statements)

References 30 publications

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“…In addition to activation of the classical pathway of complement, (35,36), urate crystals have been shown to activate HF in human plasma and synovial fluid (37). That complement participates in the pathogenesis of gout has been reported previously (33,34). In view of these findings, it is possible to postulate that activated HF may participate in the pathogenesis of this disease by either converting high molecular weight kininogen to produce bradykinin or activating the complement system to produce vasoactive peptides.…”

Section: Discussionmentioning

confidence: 64%

Activation of the classical pathway of complement by Hageman factor fragment.

Ghebrehiwet¹,

Silverberg²,

Kaplan³

1981

The Journal of Experimental Medicine

236

111

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A fragment of activated Hageman factor (HFf) has been demonstrated to activate the classical pathway of complement in a manner that is analogous to complement activation by antigen-antibody complexes or aggregated IgG. Thus C1, C4, C2, C3, and C5 were found to be depleted on addition of HFf to serum. The reduction of serum hemolytic activity was maximal upon addition of 5 micrograms HFf and an incubation time of 60 min at 37 degrees C. Consumption of the total complement activity and of the individual components proceeded in a dose-dependent fashion. No comparable activity was observed when equimolar concentrations of either the native Hageman factor (HF) or two-chain activated form of Hageman factor (HFa) were incubated with serum. Further, the ability of HFf to convert serum C3 and C4 was similar to that of aggregated IgG as assessed by immunoelectrophoresis. This function of HFf appeared to be independent of plasminogen (or plasmin) since plasminogen-free serum was indistinguishable from normal serum. Radial double immunodiffusion experiments using antiserum to C1q, C1r, and C1s on HFf-treated serum demonstrated the dissociation of the C1 trimolecular complex, with concomitant reduction of C1r antigenicity that is indicative of C1 activation. Thus, HFf appears to lead to C1 activation upon incubation with serum or when incubated with partially purified C1. This may represent a control link between activation of the intrinsic coagulation-kinin pathway and the initiation of the classical complement cascade.

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Section: Discussionmentioning

confidence: 64%

Activation of the classical pathway of complement by Hageman factor fragment.

Ghebrehiwet¹,

Silverberg²,

Kaplan³

1981

The Journal of Experimental Medicine

236

111

View full text Add to dashboard Cite

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“…It was assumed here that some direct relationship must occur between the increase in granulocytes and the development of arthritis. Reviews of the role of these cells in the onset and proliferation of many inflammatory diseases are numerous and cannot be detailed here; nevertheless, that of KELLERMEVER and NAFF [20], concerning their role in gouty arthritis of man, is sufficient background for a discussion of their probable role in adjuvant disease of the rat -another rather non-specific pathologic re- …”

Section: Discussionmentioning

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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“…It is, as Garrod had already suggested in 1859, the deposition of sodium urate crystals which is responsible for the inflammatory reaction in gout, although today we know that several factors are involved in this process (Kellermeyer and Naff, 1975). The tophus, the specific granulomatous lesion of gout, contains a variable number of urate crystals singly or in bundles, often within a necrotic or lipid core (Sokoloff, 1957).…”

Section: Articular Goutmentioning

confidence: 99%

Renal pathology of the fowl — A review

1981

Avian Pathology

149

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On the basis of published literature and some original observations a comprehensive review is presented of the current concept of renal diseases in the fowl. All aspects of this important but much neglected subject are considered including autolysis, intoxications, inflammatory and degenerative conditions, specific viral diseases, gout, congenital abnormalities and neoplasms. The aetiology and pathogenesis of some forms of avian kidney disease are well understood but there are large gaps in our knowledge on others.

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Chemical mediators of inflammation in acute gouty arthritis

Cited by 29 publications

References 30 publications

Activation of the classical pathway of complement by Hageman factor fragment.

Activation of the classical pathway of complement by Hageman factor fragment.

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

Renal pathology of the fowl — A review

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